title: The aging kidney is characterized by tubuloinflammaging, a phenotype associated with MHC-II gene expression

city: Hannover

first: Julius

last: Sinning

address: Carl-Neuberg-Str. 1

institute: Hannover Medical School

summary: We performed RNA-seq of non-irradiated and irradiated proximal tubular epithelial cells as well as RNA-seq of kidneys from different ages in order to analyze the gene expression profile of senescent tubular cells

overall_design: Comparative gene expression profiling analysis of RNA-seq data for non-irratiated and irradiated PTEC and kidneys from different ages

first: Nils

last: Funk

first: Inga

last: Soerensen-Zender

first: Vera

last: Wulfmeyer

first: Chieh

last: Liao

first: Hermann

last: Haller

first: Christian

last: Hinze

first: Kai

last: Schmidt-Ott

first: Anette

last: Melk

first: Roland

last: Schmitt


title: Fam20c regulates the calpain proteolysis system through phosphorylating Calpasatatin to maintain cell homeostasis

status: Public on Sep 11 2023

city: Guangzhou

first: Xinpeng

last: Liu

state: Guangdong

address: 157 health care road, nangang district, Harbin

department: StomatologicalHospital

country: China

institute: Southern Medical University

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Background: The family with sequence similarity 20-member C (FAM20C) kinase, a Golgi casein kinase, which is responsible for phosphorylating the majority of the extracellular phosphoproteins within S-x-E/pS motifs, and is fundamentally associated with multiple biological processes to maintain cell proliferation, biomineralization, migration, adhesion, and phosphate homeostasis. In dissecting how FAM20C regulates downstream molecules and potential mechanisms, however, there are multiple target molecules of FAM20C, particularly many phenomena remain elusive, such as changes in cell-autonomous behaviors, incompatibility in genotypes and phenotypes, and others. Methods: Here, assay for transposase-accessible chromatin using sequencing (ATAC-seq), RNA sequencing (RNA-seq), proteomics, and phosphoproteomics were performed in Fam20c-dificient osteoblasts and to facilitate an integrated analysis and determine the impact of chromatin accessibility, genomic expression, protein alterations, signaling pathway, and post translational modifcations. Results: By combining ATAC-seq and RNA-seq, we identified TCF4 and Wnt signaling pathway as the key regulators in Fam20c-dificient cells. Further, we showed Calpastatin/Calpain proteolysis system as a novel target axis for FAM20C to regulate cell migration and F-actin cytoskeleton by integrated analysis of proteomics and phosphoproteomics. Furthermore, Calpastatin/Calpain proteolysis system could negatively regulate the Wnt signaling pathway. Conclusion: These observations implied that Fam20c knockout osteoblasts would cause cell homeostatic imbalance, involving changes in multiple signaling pathways in the conduction system.

first: Lili

last: Jiang

first: Wenxuan

last: Zhang

first: Jiahui


title: FOXK2 geneknockown induces transcriptomic changes in breast cancer cell line MCF7

city: Washington

first: Yang

last: Yu

state: DC

address: 111 Michigan Ave NW

country: USA

institute: Children's national hospital

type: Expression profiling by high throughput sequencing

summary:
To investigate the effect of FOXK2 knockdown on transcriptomic profiling in breast cancer  and delineate the role of FOXK2 in breast cancer growth.
We knockdowned the gene exprssion of FOXK2 in MCF7 cells and performed gene expression profiling analysis using data obtained from RNA-seq.

overall_design:
We compared the transcriptomic change between FOXK2 knockdown groups and the control groups.  Differential gene expression (DGE) analysis of RNA-Seq was conducted with the R statistical package DESeq2 (v1.28.1).
We performed gene set analysis on DGEs by over-representation test on the ConsensusPathDB  web-portal. Genes detected in our experiments are selected on the background list.

first: Chunchao

first: Jianhua

last: Yang


title: Gene expression of MC38 tumor tissues from WT or TLR4 deletion mice during Salmonella treatment.

city: Changsha

first: Yanxia

last: Guo

address: 100 Fubuhe Street, Yuelu District

institute: Hunan University

summary: To investigate the function of host TLR4 in Salmonella-mediated cancer therapy, we established MC38 tumor-bearing  WT and TLR4 deletion mice for Salmonella treatment.

overall_design: Gene expression profiling analysis using data obtained from RNA-seq of 4 different tumor tissues after 1 day treatment.

first: Zhongying

last: Li

first: Yujie

last: Sun

first: Chaohui

last: Zuo


title: Therapeutic TNF Inhibitors Exhibit Differential Levels of Efficacy in Accelerating Cutaneous Wound Healing

city: Worcester

first: Jing

last: Wang

state: MA

address: 100 Research Drive

institute: AbbVie

summary: Adalimumab, but neither etanercept nor certolizumab-pegol, has been reported to induce a wound healing profile in the circulation of patients with hidradenitis suppurativa (HS), a chronic inflammatory skin disease. However, the role of tumor necrosis factor alpha (TNF) inhibitors in cutaneous wound healing in vivo is still unclear. To examine and compare the efficacy of various TNF inhibitors in cutaneous wound healing in vivo, a human TNF knock-in Leprdb/db mouse model was established to model the impaired cutaneous wound healing as seen in HS. The vehicle group exhibited severe impairments in cutaneous wound healing. In contrast, adalimumab significantly accelerated healing, confirmed by both histologic assessment and a unique healing transcriptional profile. Moreover, adalimumab and infliximab showed similar levels of efficacy, but golimumab was less effective, along with etanercept and certolizumab-pegol. In line with histologic assessments, proteomics analyses from healing wounds exposed to various TNF inhibitors revealed distinct and differential wound healing signatures that may underlie the differential efficacy of these inhibitors in accelerating cutaneous wound healing. Taken together, these data revealed that TNF inhibitors exhibited differential levels of efficacy in accelerating cutaneous wound healing in the impaired wound healing model in vivo likely through distinct mechanisms of action related to the structure of the biologic or its ability to bind TNF.

overall_design: Comparative gene expression profiling analysis of RNA-seq data from wounded mouse skin treated with Adalimumab or control (three biological replicates) at three timepoints.

first: Michael

middle: P

last: Macoritto

first: Yonghao

last: Cao


title: Pharmacologic inhibition of BAF chromatin remodeling complexes as a therapeutic approach to transcription factor-dependent cancers

city: Cambridge

first: Salih

last: Topal

address: 500 Technology Square Suite 700

institute: Foghorn Therapeutics

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Suspended hydrogel culture as a method to scale up intestinal organoids

city: South San Francisco

first: Kimberly

last: Homan

state: CA

address: 1 DNA Way

institute: Genentech

summary: Primary tissue-derived epithelial organoids are a physiologically relevant in vitro intestinal model that have been implemented for both basic research and drug development applications. The existing method of culturing intestinal organoids in surface-attached native extracellular matrix (ECM) hydrogel domes is not readily amenable to large-scale culture and contributes to culture heterogeneity. We have developed a method of culturing intestinal organoids within suspended basement membrane extract (BME) hydrogels of various geometries, which streamlines the protocol, increases the scalability, enables kinetic sampling, and improves culture uniformity without specialized equipment or additional expertise. We demonstrate the compatibility of this method with multiple culture formats, and provide examples of suspended BME hydrogel organoids in downstream applications: implementation in a medium-throughput drug screen and generation of Transwell monolayers for barrier evaluation. The suspended BME hydrogel culture method will allow intestinal organoids, and potentially other organoid types, to be used more widely and at higher throughputs than previously possible.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for colon organoids grown in adherent dome format or suspended BOBA under stem-like or differentiated media conditions

first: Julia

middle: Y

last: Co

first: Jessica

middle: A

last: Klein

first: Serah

last: Kang


title: Cross-species single-cell transcriptomic analysis reveals the landscape of animal gastric antrum

city: Beijing

first: Ye-guang

last: Chen

address: Tsinghua Road, Medical Building

department: School of life science

institute: Tsinghua University

sample_organism:
Homo sapiens
Sus scrofa
Mus musculus
Rattus norvegicus


title: Cross-species single-cell transcriptomic analysis reveals the landscape of animal gastric antrum [scRNA-Seq]

summary:
Purpose: To reveal the consistency and difference of gastric antrum epithelial cells among species and provides insights into the selection of model organisms in different research directions in the future.
Methods:In this study, we collected antrum epithelial tissues from human, pig, rat and mouse for scRNA-seq and conducted cross species analysis.
Results: In pig antral epithelium, we identify a novel cell cluster. We also discovered that the porcine antral epithelium owns stronger immune function than the other species. Further analysis reveals this may be due to the insufficient function of porcine immune cells.
Conclusions:Our results replenish the information of multiple species of gastric antral epithelium at the single cell level, providing data resources for understanding the basic situation of gastric antrum epithelial cells.

platform_organism:
Homo sapiens
Sus scrofa
Mus musculus
Rattus norvegicus

overall_design: Single cell profiles of gastric antrum epithelial cells from human, pig, rat and mouse

first: Ye-Guang

first: Xiaodan

first: Fan

last: Hong

first: Haonan

first: Yuan

last: Liu

first: Yalong

first: Mengxian

first: Shibo

last: Lin

first: Hui

last: Liang


title: Farnesol brain transcriptomics in CNS inflammatory demyelination

city: Boise

first: Javier

last: Ochoa-Reparaz

state: ID

address: 1910 W University Dr, Science 228 MS1515

institute: Boise State University

summary: To understand the molecular mechanisms underlying the protective neuroinflammatory activity of farnesol (FOL), we examined the transcriptomic profile of the brains of EAE mice treated with daily oral FOL using next-generation sequencing (RNA-seq).  EAE-induced mice, compared to naïve, healthy mice, overall showed increased expression in pathways for immune response, as well as increased cytokine signaling pathway, with downregulation of cellular stress proteins. Our analysis found that FOL downregulated pro-inflammatory pathways and attenuated the immune response in EAE. FOL downregulated the expression of genes involved in misfolded protein response, MAPK activation/signaling, and pro-inflammatory response.

overall_design: Total RNA from whole brains from EAE mice, EAE mice treated with FOL or with corn oil (vehicle), and naïve (healthy) mice was obtained at the peak of EAE (day 19). Transcriptomics analysis was performed in total RNA obtained from whole brains

first: William

middle: J

last: Doyle

first: Dana

last: Walters

first: Jean-Baptiste

last: Roullet


title: Melanoma-intrinsic NR2F6 activity regulates anti-tumor immunity

city: La Jolla

first: Ze'ev

middle: A.

last: Ronai

address: 10901 North Torrey Pines Road

department: Tumor Initiation and Maintenance Program, NCI-Designated Cancer Center

institute: Sanford Burnham Prebys Medical Discovery Institute

summary: Nuclear receptors (NRs) are implicated in the regulation of tumors and immune cells. We identify a tumor-intrinsic function of the orphan NR, NR2F6, regulating anti-tumor immunity. NR2F6 was selected from 48 candidate NRs, based on an expression pattern in melanoma patient specimens (i.e., IFN signature) associated with positive responses to immunotherapy and favorable patient outcomes. Correspondingly, genetic ablation of NR2F6 in a mouse melanoma model conferred a more effective response to PD-1 therapy. NR2F6 loss in B16F10 and YUMM1.7 melanoma cells attenuated tumor development in immune-competent but not -incompetent mice via the increased abundance of effector and progenitor-exhausted CD8+ T cells. Inhibition of NACC1 and FKBP10, identified as NR2F6 effectors, phenocopied NR2F6 loss. Remarkably, inoculation of NR2F6 KO mice with NR2F6 KD melanoma cells further decreased tumor growth compared with NR2F6 WT mice. Tumor-intrinsic NR2F6 function complements its tumor-extrinsic role and justifies the development of novel anti-cancer therapies.

overall_design: Gene expression comparisons of  NR2F6 KO and control in bulk tumors, MACS-sorted tumor cells, and cultured cells using RNA-seq.

first: Hyungsoo

last: Kim

first: Ze’ev


title: SETD7 promotes lateral plate mesoderm formation by modulating the Wnt/b-catenin signaling pathway

city: TianJin

first: Changlu

last: Xu

state: TianJin

address: 288 Nanjing Rd, Heping

department: State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Institute of Hematology & Blood Diseases Hospital

institute: Chinese Academy of Medical Sciences & Peking Union Medical College

summary: Investigating the role of SETD7 during human hematopoietic development

overall_design: We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different genotypes at two time points.

first: Lihong

last: Shi

first: Ding

last: Wang

first: Yapu

last: Li


title: scRNA-seq of siRNA treated hiPSC-derived islet cells

city: Leuven

first: Vincent

last: Pasque

address: Herestraat 49 bus 804

department: Development and Regeneration

country: Belgium

institute: KU Leuven

overall_design: scRNA-seq of hiPSC-derived islet cells treated with either Control siRNA, BHLHE41 siRNA or JUND siRNA 72h prior.

first: Lotte

last: Vanheer

first: Federica

last: Fantuzzi

first: San

middle: K

last: To

first: Andrea

last: Schiavo

first: Matthias

last: Van Haele

first: Tine

last: Haesen

first: Xiaoyan

last: Yi

first: Adrian

last: Janiszewski

first: Joel

last: Chappell

first: Adrien

last: Rihoux

first: Toshiaki

last: Sawatani

first: Tania

last: Roskams

first: Francois

last: Pattou

first: Julie

last: Kerr-Conte

first: Miriam

last: Cnop


title: Chronic Prenatal Delta-9-tetrahydrocannabinol Exposure Adversely Impacts DNA methylation in a Rhesus Macaque Model [methylation]

city: Beaverton

first: Lyndsey

middle: Elizabeth

last: Shorey-Kendrick

state: Oregon

address: 505 NW 185th Ave

institute: Oregon Health and Science University

summary:
Epigenome-wide profiling of DNAm in samples obtained from 10 rhesus macaques
Edibles were administered prior to the animal’s daily chow to ensure consumption on an empty stomach and to confirm complete ingestion. Animals were slowly titrated up to 2.5mg/7kg/day of THC using published weight-based medical cannabis acclimation recommendations approximately 4 months prior to undergoing time-mated breeding. Each THC-exposed pregnant animal (n=5) continued to consume a daily edible of 2.5mg/7kg/day throughout pregnancy.

overall_design: Illumina MethylationEPIC analysis performed on 5 tissues from 10 animals (5 THC; 5 CON). One heart sample (right ventricle) was not collected at necropsy. One Cerebellum sample was removed due to low signal intensity.

first: J

last: Lo

first: L


title: The transcription factor Stat-1 is essential for Schwann cell differentiation, myelination and myelin sheath regeneration

city: Nantong

first: Yun

last: Gu

state: Jiangsu

address: 19 Qixiu Road

institute: Nantong University


title: The transcription factor Stat-1 is essential for Schwann cell differentiation, myelination and myelin sheath regeneration [RNA-seq]

summary: To investigate the potential mechanisms of Stat1 regulation of Schwann cell (SC) differentiation, we performed a RNA sequencing (RNA-seq) of SCs grown under differentiation conditions treated with Stat1-siRNA or with non-targeting negative control siRNA (Scramble).

overall_design: Comparative gene expression profiling analysis of RNA-seq data for differentiating Stat1 knockdown Schwann cells and control Schwann cells.

first: Jinghui

last: Xu

first: Bin

last: Zhang

first: Wenfeng

last: Su


title: Transcriptome Regulation by PARP13 in Basal and Antiviral States in Human Cells (eCLIP)

first: Gene

last: Yeo

address: 2880 Torrey Pines Scenic Dr. Room 3805/Yeo Lab

institute: UCSD

summary: The RNA-binding protein PARP13 is a primary factor in the innate antiviral response. PARP13 can suppress translation and drive decay of bound viral and host RNA. PARP13 interacts with many proteins encoded by interferon-stimulated genes (ISG) to perform its antiviral activities, such as activation of the pathway mediated by post-translational addition ISG15 or ISGylation. The RNA-binding domains of both PARP13 and its primary cofactor, TRIM25, are required for antiviral activity. Here we perform enhanced crosslinking immunoprecipitation (eCLIP) and RNA-seq to investigate the role of PARP13 expression and RNA binding in transcriptome regulation within human cells. We find that PARP13 regulates the transcriptome in basal and antiviral states and that the antiviral response shifts PARP13 target localization, but not its binding preferences. We demonstrate that PARP13 expression supports the expression of ISGylation-related genes, including TRIM25. Using the common targets PARP13 and TRIM25 share, we assess their spatial relationship along transcripts and show that PARP13 and TRIM25 associate in part via RNA-protein interactions. Evidence from genomic data and molecular biology experiments provide insight into the geometry of PARP13's interface with its cofactor TRIM25 and implicates PARP13 in creating and maintaining a cellular environment poised for an antiviral response.

overall_design: Enhanced CLIP-seq (eCLIP) was performed on WT  cells 24 h after transfection with either an ssRNA control or a 3p-RNA viral mimic in duplicate.

first: Veronica

middle: F

last: Busa

first: Yoshinari

last: Ando

first: Stefan

last: Aigner

first: Brian

last: Yee

middle: W

first: Anthony

middle: L

last: Leung


title: The transcription factor Stat-1 is essential for Schwann cell differentiation, myelination and myelin sheath regeneration [ChIP-seq]

summary: Here, we demonstrated that the signal transducer and activator of transcription 1 (Stat1) is essential for Schwann cell (SC) differentiation. To identify genes directly targeted by Stat1, we performed chromatin immunoprecipitation sequencing (ChIP-Seq) in differentiating rat SCs.

overall_design: Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for Stat1 in differentiating rat SCs.


title: Effect of ACLY inhibition on LPS-induced EC gene profiles

city: shanghai

first: Ranran

last: Li

state: shanghai

address: ruijin hospital

institute: ruijin hospital

summary: To investigate the regulatory role of ACLY activation in EC functions, we treated HUVEC with ACLY inhibitor BMS-303141 before LPS stimuli.  We then performed gene expression profiling analysis using data obtained from RNA-seq of HUVEC lysates.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for HUVEC.


title: Cross-species single-cell transcriptomic analysis reveals the landscape of animal gastric antrum [RNA-Seq]

first: Ye-guang

last: Chen

summary:
Purpose: One goal of the bulk RNA-seq of organoids is to verify the differentially expressed genes between species identified by scRNA-seq .The other goal is to detected the differentially expressed genes when organoids from different species were treated with TNFα
Methods: The total RNA from organoids was extracted by RNeasy Mini Kit (Qiagen).  After total RNA extraction and then subjected to high-throughput sequencing on an Illumina Novaseq 6000 platform.
Results: Most of the differentially expressed genes between species identified by bulk RNA-seq are consistent with the genes filtered by scRNA-seq.
Conclusions: F3 and CLCA1 show higher expression in organoids of pig antral epithelium than in other three species. TNFα treatment upregulated the expression of immune response genes in all species

overall_design: Bulk RNA-seq of gastric antrum epithelial organoids from human, pig, rat and mouse

first: Ye-Guang

first: Xiaodan

last: Wang

first: Fan

last: Hong

first: Haonan

first: Yuan

last: Liu

first: Yalong

first: Mengxian

first: Shibo

last: Lin

first: Hui

last: Liang


title: Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium Methylation450K)

city: Chiba

first: Masaki

last: Fukuyo

address: 1-8-1 Inohana, Chuo-ku

department: Department of Molecular Oncology

country: Japan

institute: Chiba University

type: Methylation profiling by genome tiling array

summary: Comprehensive DNA methylation analysis of each histological LUAD subtype. Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across 485,577 CpG sites. Samples included 6 Micropapillary subtype, 5 Papillary subtype, 5 Lepidic subype and 3 normal lung tissues.

overall_design: Bisulphite converted DNA from the 14 samples were hybridised to the Infinium MethylationEPIC BeadChip.

first: Yuki

last: Ito

first: Genki

last: Usui

first: Keisuke

last: Matsusaka

last: Sata

first: Junichi

last: Morimoto

first: Ichiro

last: Yoshino

first: Atsushi

last: Kaneda


title: Combinatorial transcription factor binding encodes cis-regulatory wiring of forebrain GABAergic neurogenesis

city: Davis

first: Alex

middle: S.

last: Nord

address: 1544 Newton Court

department: Center for Neuroscience

institute: University of California Davis

summary: Transcription factors (TFs) bind combinatorially to genomic cis-regulatory elements (cREs), orchestrating transcription programs. While studies of chromatin state and chromosomal interactions have revealed dynamic neurodevelopmental cRE landscapes, parallel understanding of the underlying TF binding lags. To elucidate the combinatorial TF-cRE interactions driving mouse basal ganglia development, we integrated ChIP-seq for twelve TFs, H3K4me3-associated enhancer-promoter interactions, chromatin and transcriptional state, and transgenic enhancer assays. We identified TF-cREs modules with distinct chromatin features and enhancer activity that have complementary roles driving GABAergic neurogenesis and suppressing other developmental fates. While the majority of distal cREs were bound by one or two TFs, a small proportion were extensively bound, and these enhancers also exhibited exceptional evolutionary conservation, motif density, and complex chromosomal interactions. Our results provide new insights into how modules of combinatorial TF-cRE interactions activate and repress developmental expression programs and demonstrate the value of TF binding data in modeling gene regulatory wiring.

overall_design:
ChIP-seq, PLAC-seq
Peak files includes data from GSE124936, GSE85705, and GSE69724.

first: Rinaldo

last: Catta-Preta

first: Susan

last: Lindtner

first: Athena

last: Ypsilanti

first: James

last: Price

first: Linda

last: Su-Feher

first: Yurong

first: Armen

last: Abnousi

first: Yin

last: Shen

first: Axel

last: Visel

first: Len

last: Pennacchio

first: Diane

last: Dickel

first: John

last: Rubenstein


title: Discovery of extracellular vesicles derived miR-185-5p in patient’s plasma as an indicator for advanced adenoma and malignant tumor of colon

city: Shanghai

first: yunjie

last: shi

address: No 800，Xiangyin Road

institute: Naval Medical University

type: Non-coding RNA profiling by high throughput sequencing

summary: We attempted to screen and identify new plasma EV delivered microRNA can simultaneously diagnose AA, early CRC and advanced CRC in healthy people. We employed microRNA deep sequencing assay for the primary screen and performed TaqMan microRNA assay for further test and validation. Through stepwise screen and validation in two independent cohorts (cohort I: n=75, cohort II: n=104), we demonstrated that plasma EV-delivered miR-185-5p is a potential indicator of AA and CRC in Chinese patients. In the supplementary phase, we also preliminarily proved that miR-185-5p can promote the development of CRC in vivo and in vitro.

overall_design: Comparative miRNA expression profiling analysis of miRNA-seq data for plasma extracellular vesicles in healthy donor, advanced adenoma, and colorectal cancer patients.

first: Yunjie

last: Shi

first: Xinxing

last: Li

first: Zhiqian

last: Hu

first: Hao

last: Wang


title: Epigenomic analysis of Alzheimer's disease brains reveals diminished CTCF binding on genes involved in synaptic organization

city: Buffalo

first: Zhen

last: Yan

state: NY

address: 955 Main St

department: Physiology and Biophysics

institute: University at Buffalo

summary: Epigenetic aberrations are suggested to play an important role in transcriptional alterations in Alzheimer's disease (AD). One of the key mechanisms of epigenetic regulation of gene expression is through the dynamic organization of chromatin structure via the master genome architecture protein, CCCTC-binding factor (CTCF). By forming chromatin loops, CTCF can influence gene transcription in a complex manner. To find out whether genome-wide DNA binding sites for CTCF are altered in AD, we compared CTCF chromatin immunoprecipitation sequencing (ChIP-Seq) data from frontal cortex of human AD patients and normal controls (n=9 pairs, all females). We have revealed that CTCF-binding affinity on many genes is significantly reduced in AD patients, and these genes are enriched in synaptic organization, cell adhesion, and actin cytoskeleton, including synaptic scaffolding molecules and receptors, such as SHANK2, HOMER1, NRXN1, CNTNAP2 and GRIN2A, and protocadherin (PCDH) and cadherin (CDH) family members. By comparing transcriptomic data from AD patients, we have discovered that many of the synaptic and adhesion genes with reduced CTCF binding in AD are significantly reduced in their mRNA expression. Moreover, a significant overlap of genes with the diminished CTCF binding and the reduced H3K27ac is identified in AD, with the common genes enriched in synaptic organization. These data suggest that the CTCF-controlled 3D chromatin organization is perturbed in AD, which may be linked to the diminished expression of target genes, probably through changes in histone modification.

relation:
Reanalysis of: GSE188101
Reanalysis of: GSE187301
Reanalysis of: GSE187313
Reanalysis of: GSE187204
Reanalysis of: GSE187152
Reanalysis of: GSE187120
Reanalysis of: GSE187749
Reanalysis of: GSE188007
Reanalysis of: GSE187610
Reanalysis of: GSE187128
Reanalysis of: GSE175327
Reanalysis of: GSE175240
Reanalysis of: GSE187662
Reanalysis of: GSE175157
Reanalysis of: GSE187842
Reanalysis of: GSE187839
Reanalysis of: GSE187499
Reanalysis of: GSE187024
Reanalysis of: GSE187943
Reanalysis of: GSE187566
Reanalysis of: GSE187311
Reanalysis of: GSE187070
Reanalysis of: GSE187771
Reanalysis of: GSE187824
Reanalysis of: GSE187163
Reanalysis of: GSE187653
Reanalysis of: GSE187050
Reanalysis of: GSE187554
Reanalysis of: GSE187769
Reanalysis of: GSE175186
Reanalysis of: GSE187086
Reanalysis of: GSE175269
Reanalysis of: GSE187616
Reanalysis of: GSE174886
Reanalysis of: GSE187090
Reanalysis of: GSE175096

overall_design:
Differential analysis of Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for CTCF between "Alzheimer's Disease" and "No cognitive decline" groups from postmortem PFC tissue.
BAM files (not uploaded) were generated using bowtie2, BED files were generated using macs2
BigWig files were generated using BamCoverage feature in DeepTools, from BAM files
assembly: hg38

first: Prachetas

last: Patel

first: Yong

last: Ren


title: Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma

first: Masaki

last: Fukuyo

overall_design: Refer to individual Series


title: Yap signature in human neutrophils

city: Shang Hai

first: Ping

middle: Ping

last: Nie

address: Songhu Road 2005

institute: Fudan University

summary: The majority of YAP signature have been derived from epithelial and/or cancer cell lines. Here we identified the exactly genes that were regulated by Yap in human neutrophils with CUT&Tag assay. We found that the target genes of Yap in neutrophils including CD14, CD54, and EGR1 which are related to the activation of neutrophils. This study provides a framework for the Yap signature in neutrophil.

overall_design: CUT&Tag Assays to analyze the target genes of Yap in neutrophils

first: Zhaocai

last: Zhou

first: Shi

last: Jiao


title: HEY1-NCOA2 interacts with RUNX2 to induce mesenchymal chondrosarcoma [ChIP-seq]

city: Tokyo

first: Takuro

last: Nakamura

address: 3-8-31 Ariake, Koto-ku

department: The Cancer Institute

institute: Japanese Foundation for Cancer Research

summary: Mesenchymal chondrosarcoma is a high-grade malignant neoplasm characterized by biphasic growth of poorly differentiated small round cells and well differentiated cartilage. Mesenchymal chondrosarcoma affects adolescents and young adults, and the HEY1-NCOA2 fusion gene is causally associated with most cases. Here we generate a mouse model for mesenchymal chondrosarcoma by introducing HEY1-NCOA2 into mouse embryonic chondrogenic progenitors followed by subcutaneous transplantation into nude mice. HEY1-NCOA2 expression successfully induced subcutaneous tumors in 68.9% of recipients, showing biphasic morphologies and expression of Sox9, a master regulator of chondrogenic differentiation, typical to human mesenchymal chondrosarcoma. Chromatin immunoprecipitation sequencing (ChIP-seq) analyses indicated frequent inclusion of the RUNX DNA consensus sequences within HEY1-NCOA2-binding peaks. Runx2 that is important for differentiation and proliferation of the chondrocytic lineage is invariably expressed in mouse mesenchymal chondrosarcoma, and interaction between HEY1-NCOA2 and Runx2 is observed using NCOA2 C-terminal domains. This interaction promotes repression of Runx2 target genes such as Adamts4 and Mmp13 to suppress chondrocytic differentiation and cell growth of tumors, and treatment with the HDAC inhibitor Panobinostat abrogates the repression activity of HEY1-NCOA2 and Runx2 to inhibit tumor growth both in vitro and in vivo. These results demonstrate that HEY1-NCOA2 expression induces malignant transformation of chondrogenic progenitors by modulating the RUNX2-regulated transcriptional program.

overall_design: HEY1-NCOA2 was introduced by retrovirus-mediated gene transfer into mouse chondrogenic progenitors followed by subcutaneous transplantation of the cells. Subcutaneous tumors were subjected to cell culture.  ChIP-seq analysis with various antibodies.

first: Yasuyo

last: Teramura

first: Miwa

last: Tanaka


title: Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium MethylationEPIC)

summary: Comprehensive DNA methylation analysis of each histological LUAD subtype. Infinium MethylationEPIC BeadChip was used to obtain DNA methylation profiles across 850,000 CpG sites. Samples included 4 Micropapillary subtype, 5 Acinar subtype, 5 Solid subype.

overall_design: Bisulphite converted DNA from the 14 samples were hybridized to the Infinium MethylationEPIC BeadChip.

first: Yuki

last: Ito

first: Genki

last: Usui

first: Keisuke

last: Matsusaka

last: Sata

first: Junichi

last: Morimoto

first: Ichiro

last: Yoshino

first: Atsushi

last: Kaneda


title: HEY1-NCOA2 interacts with RUNX2 to induce mesenchymal chondrosarcoma

summary: This SuperSeries is composed of the SubSeries listed below.


title: Single-Cell Transcriptome Analysis Reveals Neutrophil Populations in Gastric Cancer

summary: The full neutrophil heterogeneity and function remains incompletely characterized in gastric cancer progression. Here, we profiled >21,854 mouse neutrophils with an average of 1,189 genes per cell using single-cell RNA sequencing to provide a comprehensive transcriptional landscape of neutrophil function and fate decision in tumor progression. By combining scRNA-Seq analysis with tumor model, flowcytometry, genetic mice and clinical sample, our results define four neutrophils subpopulations in gastric cancer. Importantly, we also identified the critical transcription factor for the generation of effective activated neutrophils targeted for tumor cells.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: We performed scRNA-seq analysis with bone marrow neutrophils, spleen neutrophils, blood neutrophils and tumor associated neutrophils from tumor bearing mice for 10 days, and tumor associated neutrophils from tumor bearing mice for 3 days. We also performed scRNA-seq analysis with tumor infiltrated CD45+ immune cells from WT and KO mice. Next, we detected the presence of neutrophils subpopulations in human gastric cancer by scRNA-seq of sorted human tumor infiltrated CD45+ immune cells.


title: Single cell RNA-sequencing of rat gingva with diabetic periodontitis

city: Chengdu

first: Bo

last: Zhang

state: Sichuan

address: No. 14, 3rd Section, South Renmin Road, Chengdu, Sichuan, PR China

institute: Sichuan University

summary: Using single cell-RNA sequencing, we reported structural and functional changes of gingival cellulome in diabetes-associated periodontitis, with the aim to identify distinct cell populations and functions involving in disease progression. We identified inflammation-related stromal and epithelial subpopulations that expanded in diabetes-associated periodontitis, creating distinct immune microenvironment that drives the progression of the disease.

overall_design: Diabetes was induced by single intraperitoneal injection of streptozotocin in Sprague-Dawley (SD) rats. Rats in normoglycemic groups (Ctrl) received injection of vehicle. Seven days later, rats with non-fasting blood glucose levels ≥250 mg/dl were allocated to diabetic group (DM). Periodontitis was induced by ligature around second maxillary molars.  Gingiva samples were collected from four groups, normoglycemic rats without periodontitis; normoglycemic rats with periodontitis; diabetic rats without periodontitis; diabetic rats with periodontitis, and went through single cell RNA-sequencing. Each group was a mixture of 9 biological replicates.

first: Guanyin

last: Zhu


title: Transcriptome profiling from Wild Type and PLSCR1 transgenic mouse(PLSCR1-TG)retina with acute ocular hypertension (AOH) treatment reveals the  potential mechanism  involved in glaucoma

city: GaungZhou

first: Minglei

last: Zhao

address: 7#, Jinsui Road

institute: Sun yat sen university

summary: Glaucoma is a leading cause of irreversible blindness worldwide. In pathogenesis of glaucoma, the molecular mechanisms remain largely unknown. Phospholipid scramblase 1 (PLSCR1) is a key regulator promoting RGCs apoptosis and their clearance by microglia. As evidenced in RGCs of PLSCR1 transgenic mice model treated with acute ocular hypertension, transcriptome profiling from Wild Type and PLSCR1 transgenic mouse(PLSCR1-TG)retina with AOH treatment would reveal the  potential mechanism  involved in glaucoma.

overall_design: RNA-seq profiles of retina from WT and PLSCR1-TG after AOH treatment after 5 days

first: Ling

first: Jingyi

last: Luo

first: Qing

last: Lian


title: Characterization of Global DNA Methylome in Mild Cognitive Impairment and Alzheimer's Disease

first: Shan

last: Chao

address: Huashan Rd, No. 2018

institute: Shanghai Decoding Research Institute

summary: Genome-wide profiling of DNA methylation in blood leukocytes from Chinese patients with mild cognitive impairment (MCI) and Alzheimer’s disease (AD). The Illumina Infinium MethylationEPIC BeadChip array (850K chip) was used to detect DNA methylation profiles throughout approximately 850,000 CpG sites in peripheral blood white cells of MCI- and AD-affected Chinese patients, as well as cognitively healthy controls. All samples included 20 Chinese patients with MCI, 20 Chinese patients with AD, and 20 cognitively healthy controls.

overall_design: Genomic DNA was converted by bisulphite, and subsequently hybridised to the Illumina Infinium MethylationEPIC BeadChip.

first: Shaochang

last: Wu

first: Fan

last: Yang

first: He

last: Li

first: Limei

last: Yu

first: Lin

last: He

first: Xingwang

first: Liya

last: Sun

first: Shengying

last: Qin


title: Long non-coding RNA Mir17hg positively regulates melanogenesis by inhibiting TGFβ receptor 2 under psychological stress

status: Public on Sep 10 2023

city: NANJING

first: zan

last: peng

state: JIANGSU

address: 2F, Building 3, South District, Life Science and Technology Town, No. 18, Zhilan Road, Jiangning District

institute: CHINA PHARMCUTICAL UNIVERSITY

summary: Skin is the largest organ and it communicates with the brain through neural and humoral signals. Stress has been demonstrated to be the main cause of unhealthy hair cycles and depigmentation. In this study, We used a mouse model for chronic restraint stress (CRS) to observe its effect on pigmentation. After 12 weeks under stress, total RNA was extracted from the dorsal skin of three mice in each group. We uncovered 1,047 differentially expressed genes. Among these, 101 differentially expressed Long non-coding RNAs (lncRNAs) were identified. Further, we explored the effect of lncRNA Mir17hg on melanin production in vivo and in vitro, and proved that Mir17hg promotes melanogenesis by inhibiting TGFβR2.

overall_design: RNA was extracted from skin of CRS mice (n = 3) and CON mice (n = 3) after 12 weeks under stress.

first: Jing

last: Dong

first: Zan

last: Peng

first: Minghan

last: Chen

first: Yifan

last: Lai

first: Xiaofeng

first: Meng

first: Hui

last: Zhong

first: Jun

last: Liu

first: Yunyun

last: Yue

last: Shang


title: GSE1 promotes the proliferation and migration of lung adenocarcinoma cells by downregulating KLF6 expression

city: Hefei

first: YiXuan

address: 81 Meishan Road

institute: Anhui Medical University

summary: Background: Lung cancer, particularly lung adenocarcinoma, remains one of the most lethal malignancies globally. Identifying aberrant molecular pathways and potential therapeutic targets is pivotal for improving patient outcomes. This study focused on the role of GSE1 (genetic suppressor element 1) in lung adenocarcinoma, elucidating its interaction mechanisms and downstream effects. Objectives: 1. Determine the expression levels of GSE1 in lung adenocarcinoma tissues and its implication on cancer cell behaviors. 2. Investigate the effects of GSE1 depletion on the proliferation and migration capabilities of A549 and H1299 lung adenocarcinoma cell lines. 3. Elucidate the potential cellular partners of GSE1, with a particular focus on its interaction with histone deacetylase 1 (HDAC1) and the broader BRAF-HDAC complex (BHC). 4. Analyze the transcriptomic changes following GSE1-knockdown in A549 cells to pinpoint its broad molecular influence. 5. Examine the possible cooperative role of GSE1 and HDAC1 in modulating the expression of significant genes, especially the tumor suppressor gene KLF6. Methods: GSE1 expression was assessed in lung adenocarcinoma tissues and correlated with cell behaviors. The effects of GSE1 depletion were studied in A549 and H1299 cells. Immunoprecipitation assays were utilized to confirm GSE1's interactions. Transcriptomic analysis identified differentially expressed genes post-GSE1-knockdown, with a focus on genes harboring HDAC1 binding sites. The relationship between GSE1 and KLF6 expression was verified using RT-qPCR and western blotting. Results: GSE1 was found to be upregulated in lung adenocarcinoma. Its depletion inhibited proliferation and migration in both A549 and H1299 cells. GSE1 was demonstrated to interact with HDAC1 and other BHC components. Following GSE1-knockdown, 207 genes were upregulated and 159 were downregulated, with 140 genes showcasing HDAC1 binding sites. Among these genes, GSE1 was revealed to inhibit the transcription of the tumor suppressor gene KLF6. Conclusion: GSE1 plays a central role in promoting non-small cell lung cancer progression, potentially through its cooperation with HDAC1. This interaction appears to downregulate KLF6 expression, highlighting a novel molecular pathway that can be targeted for therapeutic interventions in lung adenocarcinoma.

overall_design: Objective: The primary goal of this experiment is to understand the effects of GSE1 knockdown on the transcriptome of A549 cells and identify the genes and pathways influenced by GSE1. 1. Sample Preparation: - Cell Type: Human lung adenocarcinoma cell line, A549. Sample Groups:  GSE1-knockdown: A549 cells transfected with GSE1 siRNA, designed to specifically reduce the expression of GSE1. Control: A549 cells transfected with negative control siRNA, which should not interfere with the gene expression and serves as a comparison baseline. Culturing Conditions: Cells were cultured in 6-well plates with a seeding density of 2 × 10^5 cells/well. After 24 hours of growth, cells underwent transfection. 2. Transfection: Following 24-hour growth, A549 cells were transfected with either GSE1 siRNA (for GSE1 knockdown) or negative control siRNA. 48 hours post-transfection, cells were washed with PBS to prepare for RNA extraction. 3. RNA Extraction and Validation: Total RNA was isolated from both sample groups using the TRIzol reagent. The extracted RNA's quantity and integrity were validated using a NanoDrop One Microvolume UV-Vis Spectrophotometer. The effectiveness of GSE1 knockdown at the protein level was confirmed via western blotting. 4. RNA Sequencing: From the validated RNA samples, cDNA libraries were prepared using the TruSeq RNA Sample Preparation Kit. These libraries were then sequenced on a HiSeq 4000 instrument, generating paired-end reads (50SE) at a depth of approximately 20 million sequences. 5. Data Processing and Analysis: Initial raw sequencing data underwent quality control to remove low-quality reads, adapters, and Poly-N sequences. Cleaned reads were then mapped to the human reference genome using STAR software, allowing a maximum of two mismatches per read. The expression levels of genes (quantified as RPKM) were determined, followed by the identification of differentially expressed genes (DEGs) between the GSE1-knockdown and control groups using DESeq2 software. Significant DEGs were filtered based on a false discovery rate (FDR) ≤ 0.001 and a difference in RPKM ratio ≥ 0.5.

first: Ziyu

last: Meng

first: Yingqian

first: Liguo

last: Huang

first: Zhoujuan

last: Yao

first: Yixuan

first: Junkun

last: Wang

first: Yiru

last: Shen

first: Pingping

last: Liang

last: Zhang

first: Fengsong

first: Wenbin


title: Linker histones mediate sequence-specific regulation of chromosomal organization and H3K27me3 enrichment over genes and telomeric repeats [TRB1-GFP ChIP-seq]

city: Paris

first: Fredy

last: BARNECHE

address: Rue d'Ulm

department: IBENS

country: France

institute: CNRS

summary: Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.

overall_design: Chromatin immunoprecitation (ChIP-seq) analysis of TRB1 genome distribution in WT and 2h1 plants

first: Lorenzo

last: Concia

first: Léa

last: Wolff

first: Clara

last: Bourbousse

last: Barneche


title: Adult Mouse Leptomeninges Exhibit Regional and Age-related Cellular Heterogeneity Implicating Mental Disorders

city: Rensselaer

first: Farhad

last: Farjood

address: 1 Discovery Drive

institute: Neural Stem Cell Institute

summary: Transplantation of retinal pigment epithelial (RPE) cells holds great promise for RPE tissue repair in patients with retinal degenerative diseases, such as age-related macular The leptomeninges envelop the central nervous system (CNS) and contribute to cerebrospinal fluid (CSF) production and homeostasis. We analyzed  the meninges overlying the anterior or posterior forebrain in the adult mouse by single nuclear RNA-sequencing (snucRNA-seq). This revealed regional differences in fibroblast and endothelial cell composition and gene expression. Surprisingly, these non-neuronal cells co-expressed genes implicated in neural functions. The regional differences changed with aging, from 3  to 18 months. Cytokine analysis revealed specific soluble factor production from anterior vs posterior meninges that also altered with age. Secreted factors from the leptomeninges from different regions and ages differentially impacted the survival of anterior or posterior cortical neuronal subsets, neuron morphology, and glia proliferation.  These findings suggest that meningeal dysfunction in different brain regions could contribute to specific neural pathologies.  The disease-associations of meningeal cell genes differentially expressed with region and age were significantly enriched for mental and substance abuse disorders.

overall_design: Anterior and posterior leptomeninges tissues were isolated from six young (3 months) and six old (18 months) mice. Tissue lysis and nuclei isolation were performed and single cell library preparation was performed using the SMART-Seq ICELL8 Application Kit.

first: Christina

last: Allen

first: Susan

last: Goderie

first: Mo

first: Thomas

middle: R

last: Kiehl

first: Yue

first: Nathan

middle: C

last: Boles

first: Sally

last: Temple


title: HEY1-NCOA2 interacts with RUNX2 to induce mesenchymal chondrosarcoma [Array]

first: Takuro

last: Nakamura

summary:
Mesenchymal chondrosarcoma is a high-grade malignant neoplasm characterized by biphasic growth of poorly differentiated small round cells and well differentiated cartilage. Mesenchymal chondrosarcoma affects adolescents and young adults, and the HEY1-NCOA2 fusion gene is causally associated with most cases. Here we generate a mouse model for mesenchymal chondrosarcoma by introducing HEY1-NCOA2 into mouse embryonic chondrogenic progenitors followed by subcutaneous transplantation into nude mice. HEY1-NCOA2 expression successfully induced subcutaneous tumors in 68.9% of recipients, showing biphasic morphologies and expression of Sox9, a master regulator of chondrogenic differentiation, typical to human mesenchymal chondrosarcoma. Chromatin immunoprecipitation sequencing (ChIP-seq) analyses indicated frequent inclusion of the RUNX DNA consensus sequences within HEY1-NCOA2-binding peaks. Runx2 that is important for differentiation and proliferation of the chondrocytic lineage is invariably expressed in mouse mesenchymal chondrosarcoma, and interaction between HEY1-NCOA2 and Runx2 is observed using NCOA2 C-terminal domains. This interaction promotes repression of Runx2 target genes such as Adamts4 and Mmp13 to suppress chondrocytic differentiation and cell growth of tumors, and treatment with the HDAC inhibitor Panobinostat abrogates the repression activity of HEY1-NCOA2 and Runx2 to inhibit tumor growth both in vitro and in vivo. These results demonstrate that HEY1-NCOA2 expression induces malignant transformation of chondrogenic progenitors by modulating the RUNX2-regulated transcriptional program.
We used microarrays to detail the global program of gene expression in mouse mesenchymal chondrosarcoma

overall_design: Murine mesenchymal chondrosarcoma cells and embryonic chondrogenic progenitor cells expressing HEY1-NCOA2

first: Yasuyo

last: Teramura


title: Effects of different forms of Anthocyanins on growth inhibition and gene expression of CRC cells

city: Shenzhen

first: Epigenomics

last: Gao

address: Dapeng district

department: Agricultural Genomics Institute at Shenzhen

institute: Chinese Academy of Agricultural Sciences

summary: Scope: Anthocyanins from diet were found to have therapeutic potential for various cancers including colorectal cancer (CRC). Given the diverse forms of anthocyanins, it is unclear whether different types of anthocyanins share common pathways in regulating intestinal cell function. This study aims to investigate the core gene pathways modulated by anthocyanins in intestinal cells, and to identify potential compounds with similar therapeutic effects.Methods and results: Three different forms anthocyanins were used to treat CRC cells at different concentrations and time points, and growth inhibition was observed in all anthocyanins, with varying patterns. RNA-seq analysis showed that the regulatory-pathways of anthocyanins with different structures were different, and the time factor had a greater effect. Time-series analysis of regulatory-genes shared by different concentrations and structures of anthocyanins was performed. By overlapping with public PPAR target gene set, a core gene set across three types of anthocyanins was identified and used in Connectivity Map (CMap) analysis to screen for compounds. The repositioned drug candidates included known anti-cancer drugs that have effects of transcriptome interventions similar to anthocyanins.Conclusion: These findings provide new insights into the mechanisms underlying the anti-CRC effects of anthocyanins and may facilitate the development of novel therapeutic agents for CRC.

overall_design: To investigate the inhibitory effect of anthocyanins on the growth of colorectal cancer cells, we treated HT29 cell line with three different concentrations and durations of anthocyanins, and conducted CCK8 assay. To explore the regulatory role of anthocyanins on the whole-genome gene expression, we analyzed the gene expression profiles of HT29 cells treated with three different concentrations of anthocyanins at two time points using RNA-seq data. This research aims to uncover the potential shared molecular mechanisms by which anthocyanins exert their anti-colorectal cancer effects through the PPAR pathway.


title: microRNA microarray profile  analysis in esophageal squamous cell carcinoma(ESCC) and adjacent normal tissues

city: Anyang

first: Yaowen

state: Henan

address: No. 1 Huanbin North Road, Beiguan District

department: Radiotherapy

institute: Anyang Cancer Hospital

summary: The miRNA expression profile related to ESCC in high-incidence areas of China was successfully constructed, and differentially expressed miRNAs were screened out and  their functions were predicted.The miRNA expression in ESCC tissues was significantly different from that in  adjacent normal tissues.GO and Pathway analysis showed that differentially expressed miRNAs were mainly involved in biological functions such as cellular process, metabolic process, biological regulation, binding and catalytic activity, and involved in multiple regulatory pathways including extracellular matrix receptor interaction, adhesion spot, protein digestion and absorption.Then their circRNA-miRNA network was constructed to better understand the related mechanism of miRNAs and provide ideas for exploring the biology functions of miRNAs in ESCC, revealing that the differentially expressed miRNAs were closely related to ESCC.

overall_design: Pairs of ESCC tissues and normal adjacent tissues were selected, and gene chip technology and microarray analysis were used to construct the miRNA expression profile. Differentially expressed miRNAs were screened with FC ≥ 2 times and p < 0.05. The functions of miRNA were predicted by GO and Pathway analysis. The circRNA-miRNA network was constructed to investigate the mechanism of miRNA.

first: Fuyou

last: Zhou


title: DNA methylation analysis in esophageal squamous cell carcinoma(ESCC) and adjacent normal tissues

summary: DNA methylation related to ESCC in high-incidence areas of China was successfully constructed, and differentially DNA methylation were screened out and  their functions were predicted.The DNA methylation in ESCC tissues was significantly different from that in  adjacent normal tissues.

overall_design: Pairs of ESCC tissues and normal adjacent tissues were selected, and gene chip technology and microarray analysis were used to construct DNA methylation.


title: Linker histones mediate sequence-specific regulation of chromosomal organization and H3K27me3 enrichment over genes and telomeric repeats

first: Fredy


title: Analysis in esophageal squamous cell carcinoma(ESCC) and adjacent normal tissues

type:
Expression profiling by array
Methylation profiling by array
Non-coding RNA profiling by array


title: HEY1-NCOA2 expression induces mesenchymal chondrosarcoma interacting with Runx2 [single-cell RNA-seq]

summary: Mesenchymal chondrosarcoma is a high-grade malignant neoplasm characterized by biphasic growth of poorly differentiated small round cells and well differentiated cartilage. Mesenchymal chondrosarcoma affects adolescents and young adults, and the HEY1-NCOA2 fusion gene is causally associated with most cases. Here we generate a mouse model for mesenchymal chondrosarcoma by introducing HEY1-NCOA2 into mouse embryonic chondrogenic progenitors (eSZ) followed by subcutaneous transplantation into nude mice. HEY1-NCOA2 expression in eSZ cells successfully induced subcutaneous tumors in 68.9% of recipients, showing biphasic morphologies and expression of Sox9, a master regulator of chondrogenic differentiation. Chromatin immunoprecipitation sequencing analyses indicated frequent association between HEY1-NCOA2-binding peaks and active enhancers. Runx2 that is important for differentiation and proliferation of the chondrocytic lineage is invariably expressed in mouse mesenchymal chondrosarcoma, and interaction between HEY1-NCOA2 and Runx2 is observed using NCOA2 C-terminal domains. Whereas Runx2 knockout resulted in significant delay in tumor onset, aggressive growth of immature small round cells was induced. Treatment with the HDAC inhibitor panobinostat suppressed tumor growth both in vitro and in vivo, abrogating expression of genes downstream of HEY1-NCOA2 and Runx2. Thus, HEY1-NCOA2 expression induces malignant transformation by modulating the transcriptional program in chondrogenic differentiation.

overall_design: HEY1-NCOA2 was introduced by retrovirus-mediated gene transfer into mouse chondrogenic progenitors followed by subcutaneous transplantation of the cells. Subcutaneous tumors were subjected to cell culture.

first: Miwa

last: Tanaka

first: Mizuki

last: Homme


title: Mechanisms of triptolide's anti-pancreatic cancer effects through inhibition of autophagy and extracellular matrix activation

status: Public on Sep 09 2023

city: NanJing

first: Jianxiang

last: GU

state: JiangSu

address: 321 Zhongshan Road

department: Department of Gastroenterology

institute: Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine

summary: Pancreatic cancer is characterized by high mortality and poor treatment.Triptolide, a natural compound derived from the traditional Chinese medicine Thunder God Vine, has shown anti-tumor activity in various cancers. This study aimed to investigate the impact of triptolide on the growth of pancreatic cancer cells and the activation of cancer-associated fibroblasts (CAFs). The findings demonstrated that triptolide effectively inhibited the proliferation of pancreatic cancer cells and the activation of CAFs. Further investigations revealed that triptolide suppressed autophagy and induced apoptosis in pancreatic cancer cells by inhibiting the secretion of CXCL1. Additionally, it inhibited tumor cell stroma formation by suppressing the paracrine secretion of TGF-β1. In conclusion, triptolide exerted its inhibitory effects on pancreatic cancer cell growth and stromal cell activation through the inhibition of CXCL1 and TGF-β1.

overall_design: The NC group cultured Miapaca-2 cells in DMEM medium containing 10% FBS for 24 hours, while the control group treated Miapaca-2 cells with 10nM triptolide for 24 hours to evaluate the changes in MRNA transcription in the control group compared to the NC group

first: Hongzhen

last: LI


title: Linker histones mediate sequence-specific regulation of chromosomal organization and H3K27me3 enrichment over genes and telomeric repeats (RNA-Seq)

last: BARNECHE

overall_design: Examination of gene expression (RNA-seq) in WT and 2h1 plants.

first: Clara

first: Lorenzo

last: Concia

first: Léa

last: Wolff


title: Linker histones mediate sequence-specific regulation of chromosomal organization and H3K27me3 enrichment over genes and telomeric repeats (Hi-C)

overall_design: Examination of 3D genome organization in WT and 2h1 plants by high throughput chromosome conformation capture (Hi-C).

first: Gianluca

last: Teano

first: Léopold

last: Carron

first: Ueli

last: Grossniklaus

first: Alessandra

last: Carbone

last: Bourbousse

first: Stefan

last: Grob

last: Barneche


title: The SGLT2 inhibitor canagliflozin suppresses growth and enhances prostate cancer response to radiotherapy

city: Hamilton

first: Amr

middle: Mohamed Ahmed

last: Ali

state: ON

address: 699 concession street-4-212

department: Oncology

country: Canada

institute: Mcmaster University

summary: Radiotherapy (RT) is a non-invasive standard treatment for prostate cancer (PC). However, PC develops radio-resistance, highlighting a need for agents to improve RT response. Canagliflozin, an inhibitor of sodium-glucose co-transporter-2, is approved for use in diabetes and heart failure, but is also shown to inhibit PC growth. However, whether canagliflozin can improve RT response in PC remains unknown. Here, we show that well-tolerated doses of canagliflozin suppress proliferation and survival of androgen-sensitive and insensitive human PC cells and tumors and sensitize them to RT. Canagliflozin blocks mitochondrial respiration, promotes AMPK activity, inhibits the MAPK and mTOR-p70S6k/4EBP1 pathways, activates cell cycle checkpoints, and inhibits proliferation in part through HIF-1𝛼 suppression. Canagliflozin mediates transcriptional reprogramming of several metabolic and survival pathways known to be regulated by ETS and E2F family transcription factors. Genes downregulated by canagliflozin are associated with poor PC prognosis. This study lays the groundwork for clinical investigation of canagliflozin in PC prevention and treatment in combination with RT.

overall_design: In this study, RNAseq was designed to examined canagliflozin’s anti-tumor mechanism of action alone and in combination with radiotherapy in CRPC and mCRPC models of prostate cancer.

first: Bassem

last: Mekhaeil

first: Olga-Demetra

last: Biziotis

first: Evangelia

middle: E

last: Tsakiridis

first: Elham

last: Ahmadi

first: Jianhan

last: Wu

first: Simon

last: Wang

first: Kanwaldeep

last: Singh

first: Gabe

last: Menjolian

first: Thomas

last: Farrell

first: Aruz

last: Mesci

first: Stanley

last: Liu

first: Tobias

last: Berg

first: Jonathan

last: Bramson

first: Gregory

last: Steinberg

first: Theodoros


title: Seasonal Light Hours Modulate Peripheral Clocks and Energy Metabolism in Mice

city: Copenhagen

first: Lewin

last: Small

address: Blegdamsvej 3B

department: CBMR

country: Denmark

institute: University of Copenhagen

summary: With the exception of latitudes close to the equator, seasonal variation in light hours can change dramatically between summer and winter. Yet, investigations into the interplay between energy metabolism and circadian rhythms typically use a 12 h light:12 h dark photoperiod corresponding to light duration at the equator. Here, we hypothesised that altering seasonal photoperiod affects both rhythmicity of peripheral tissue clocks as well as processes involved in energy storage and utilisation. Male mice were housed at one of three photoperiods representing light hours in summer, winter and the equinox. Mice housed at a winter photoperiod exhibited an increase in the amplitude of rhythmic lipid metabolism and a modest reduction in fat mass and liver triglyceride content. Comparing melatonin proficient and deficient mice, we provide evidence that the effect of seasonal light on energy metabolism is largely driven by differences in the rhythmicity of food intake, but not melatonin. Our results show that seasonal light impacts energy metabolism in mice and suggest that these effects are partly driven by modulating the timing of eating. Our work sets a course to integrate seasonal light duration in future circadian biology studies.

overall_design: RNAseq of livers from 32 male high fat diet fed C3H/HeNCrl mice, sampled every 6 hours over one full cycle, living in either short light or long light photoperiod, n = 4 per photoperiod per timepoint.

first: Leonidas

middle: S

last: Lundell

first: Romain

last: Barres

first: Juleen

last: Zierath


title: Transcriptional Characterization of Early Esophageal Squamous Cell Carcinoma

first: Shenglin

last: Huang

address: 270 Dongan

summary: To investigate the transcriptional characterization of early esophageal squamous cell carcinoma (ESCC), we performed RNA-sequencing of 10 matched pairs of tumor and adjacent normal tissues of early stage of ESCC patients

overall_design: Total RNAs (500 ng) from ESCC tissues and matched normal tissues were extracted by Trizol® Reagent (Thermo, USA) and treated with DNase I (NEB) to remove DNA before constructing the RNA-seq libraries. Strand-specific RNA-seq libraries were prepared using the QIAseq FastSelect–rRNA HMR (Qiagen) and KAPA RNA HyperPrep (Roche) kits.The libraries were quality controlled with Qubit (Thermo Fisher Scientific, USA) and Qsep100 (BiOptic, China) and sequenced by the Illumina sequencing platform (Nova) on a 150 bp paired-end run.

first: Caiping

last: Li


title: Linker histones mediate sequence-specific regulation of chromosomal organization and H3K27me3 enrichment over genes and telomeric repeats (ChIP-Seq)

first: Fredy

last: BARNECHE

overall_design: Examination of H1 and H3 occupancy in WT and 2h1 plants using chromatin immunoprecitation (ChIP-seq)

first: Clara

last: Bourbousse

first: Lorenzo

last: Concia

first: Léa

last: Wolff

last: Barneche


title: Linker histones mediate sequence-specific regulation of chromosomal organization and H3K27me3 enrichment over genes and telomeric repeats (ATAC-Seq)

overall_design: Examination of chromatin accessibility in WT and 2h1 plants by ATAC-seq.

first: Gianluca

last: Teano


title: Linker histones mediate sequence-specific regulation of chromosomal organization and H3K27me3 enrichment over genes and telomeric repeats (ChIP-RX)

overall_design: Examination of H3K27me3 marking in WT, 2h1 and 2h1-trb123 mutant plants using chromatin immunoprecitation (ChIP-seq)

first: Lea

first: Ivona

last: Biocanin


title: lncRNAs and mRNAs expression data in esophageal squamous cell carcinoma(ESCC) and adjacent normal tissues

first: Yaowen

last: Zhang

type:
Expression profiling by array
Non-coding RNA profiling by array

summary: The differential expression profile of lncRNAs and mRNAs in esophageal squamous cell carcinoma in high-incidence areas of China was constructed and co-expression correlation analysis was performed. The expression profile of lncRNAs in ESCC tissues was significantly different from that in adjacent normal tissues. Co-expression analysis revealed that lncRNA may be involved in the occurrence and development of esophageal cancer, thus providing a new basis for the diagnosis and treatment of esophageal cancer.

overall_design: Esophageal squamous cell carcinoma (ESCC) and matched adjacent normal tissues were taken, and the differential expression profiles of lncRNAs of esophageal squamous cell carcinoma (ESCC) were analyzed by microarray, and co-expression correlation analysis was performed to predict transcription factors of target genes, as well as GO and Pathway enrichment analysis.

first: Fuyou

last: Zhou


title: Arabidopsis CURLY LEAF functions in leaf immunity against fungal pathogens by concomitantly repressing SEPALLATA3 and activating plant defensins

city: Kanazawa

first: Takumi

last: Nishiuchi

address: 13-1 Takaramachi

institute: Kanazawa University

summary: Transcriptome analysis to identify genes up- and down-regulated genes in pen2 plants compared with ora59-SEP3OX plants in the case of Colletotrichum tropicale inoculation.

overall_design: In total 8 samples (four biological replicates of Colletotrichum tropicale- treated pen2 and ora59-SEP3OX plant samples) were used

first: Ayumi

last: Kosaka

first: Yoshitaka

last: Takano


title: Enhanced glutathione levels confer resistance to apoptotic and ferroptotic programmed cell death in NEIL DNA glycosylase deficient HAP1 cells

status: Public on Sep 08 2023

city: Trondheim

first: Magnar

last: Bjørås

address: Erling Skjalgssonsgate 1

department: Department of Clinical and Molecular Medicine (IKOM)

country: Norway

institute: Faculty of Medicine and Health Sciences,NTNU

summary: The NTHL1 and NEIL1-3 DNA glycosylases are major enzymes in the removal of oxidative DNA base lesions, via the base excision repair (BER) pathway. To investigate their interplay in human cells, we engineered single, double, triple, and quadruple DNA glycosylase deficient HAP1 cells using the Crisp-cas 9 technology. We found that these DNA glycosylase deficient cells are more resistant to oxidative stress caused by genotoxic agents than wild type cells, and a further augment in resistance was observed upon inhibition of glutathione synthesis. Gene expression analysis revealed that GSH depletion activates the NRF2/KEAP1 pathway and ER stress induced apoptosis. Furthermore, glutathione depleted NEIL triple KO cells are also more resistant to cell death induced via ferroptosis than wild type cells. Finally, we observed higher basal level of glutathione and differential expression of NRF2-regulated genes associated with glutathione homeostasis in these cells. We propose that NEIL deficiency leads to aberrant transcription and subsequent errors in protein synthesis, which cause ER- and proteotoxic stress. This triggers the unfolded protein response, which consequently upregulates intracellular antioxidant defence mechanisms. Altogether, our data suggest that NEIL deficient cells developed an oxidative stress defence mechanism termed hormesis mediated by elevated GSH levels in response to the increased intracellular stress inflicted by loss of NEIL123 activities.

overall_design: A panel of HAP1 cells deficient for the DNA glycosylases NEIL11, NEIL2, and NEIL3 were treated after 4h with 200µM BSO or media alone for 48 h. The total RNA was isolated for transcriptome profiling.


title: Tet2-mediated epigenetic modifications during aging of hematopoietic stem and progenitor cells

city: Shanghai

first: Shengli

address: 650 Xinsongjiang Road

institute: Shanghai Jiao Tong University School of Medicine

summary: we compared self-renewal and lineage specification of WT and Tet2-deficient HSPCs during ageing and demonstrated that Tet2 ablation alters age-dependent HSC functional decline, revealing a disparate ageing process in the Tet2-deficient haemopoietic system.

overall_design: We collected hematopoietic progenitor and stem cells (HSPCs) from young and aged WT/ Tet2KO mice for scRNA-seq analysis. CD45.2+Lin-ckit+Sca-1+ cells harvested from bone marrow transplanted mice (using hematopoietic progenitor and stem cells from young and aged WT/ Tet2KO mice as donors) were collected from SMART-RNA seq

first: Tingting

last: Hong

first: Shaohai

last: Fang

first: Anna

middle: G

last: Guzman

first: Wei

last: Han

first: Yubin

first: Margaret

last: Goodell

first: Leng

first: Yun


title: A single-cell transcriptomic atlas of mouse pituitary aging

city: Gwangju

first: Yunwon

last: Kang

state: Other

address: 123, Cheomdangwagi-ro, Buk-gu, Gwangju, Republic of Korea

department: Biomedical Science and Engineering

country: South Korea

institute: Gwangju Institute of Science and Technology

summary: Aging is a multifactorial process with significant functional alterations of the human body including endocrinal systems which control the whole-body physiology and metabolism. In this vein, aging-induced decline of endocrine function are associated with multiple physiological and metabolic diseases. However, aging-associated molecular shifts in the pituitary gland, the central organ of the endocrine system, have not been dissected systemically. In this study, we conducted single-cell transcriptomic analysis of the anterior pituitary gland by comparing old and young male mice. Single-cell transcriptomics not only increased the resolution for clustering of various cell types in the pituitary gland, but also enabled detailed analysis of differential expression and intercellular communication caused by aging. In summary, our study constructed the first single-cell transcriptomic atlas of pituitary aging and identified associated features of in a single-cell level, providing resources to develop novel potential therapeutic targets for aging-associated endocrine dysfunction.

overall_design: To investigate the aging-associated transcriptomic changes of mouse pituitary in a single-cell level, ten pituitary glands of male C57BL/6 mice were harvested from each of two distinct age groups, young (2-month) and old (20-month). Then, ten tissues from each age group were merged into a sample to secure enough number of cells for scRNA-seq

first: Yun-Won

first: Soohyun

last: Lee

first: Yumin

last: Kim

first: Eun

first: Chang-Myung

last: Oh

first: Cheol

last: Ku


title: Single cell RNA analysis reveals the complex heterogeneity of CD4+ T cells in chronic neuroinflammation

city: Berlin

first: Cornelius

last: Fischer

state: Berlin

address: Robert-Rössle-Straße 10

department: Berlin Institute for Medical Systems Biology

country: Germany

institute: Max Delbrück Center for Molecular Medicine (MDC)

summary: Multiple sclerosis (MS) is a severe chronic inflammatory disease of the central nervous system (CNS) that leads to disability in young adults. T lymphocytes are a key component of lesion pathology throughout the disease course. Here we used the animal model experimental autoimmune encephalomyelitis (EAE) to conduct an unbiased characterization of CD4+ T cells in acute and chronic EAE.

overall_design: We identified five distinct CNS CD4+ T cell populations, of which three have not yet been characterized in EAE: innate-like CD4+ T cells (Ccl5, Gzmk, NKG7), tissue resident memory T cells (Cxcr6, Bhlhe40) and lymphoid-tissue like T cells (Klf2, S1pr1, Sell).

first: Tadhg

last: Crowley

first: Kamil

last: Rosiewicz

first: Janis

last: Kerkering

first: Marlen

last: Alisch

first: Volker

last: Siffrin


title: Dihydroartemisinin inhibits the proliferation of multiple myeloma cancer stem cells via disturbing nuclear lamina and chromatin architecture

city: Beijing

first: Ying

last: Li

state: AL

address: Beijing Chaoyang Hospital

institute: 首都医科大学附属北京朝阳医院

summary: We establish a method to reprogram bulk multiple myeloma (MM) cancer cells into MM cancer stem cells (MMSCs) via heterochromatin modulation, which allows us to obtain sufficient functional MMSCs in an efficient manner. Characterization of these induced MMSCs demonstrates that the reprogrammed MMSCs possess the properties of cancer stem cells both phenotypically and functionally. To leverage this model therapeutically, we screened a panel of compounds, and identified dihydroartemisinin (DHA) as a potent anti-MMSCs drug both in vitro and in vivo. DHA induces anti-proliferation effects on MMSCs via nuclear lamina perturbation and chromatin structure alteration. Hi-C analysis reveals that DHA modulates chromatin architecture mainly at the compartmental level and TADs (topologically associating domains) level. The potent anti-MMSCs efficacy and the novel molecular insights establish the therapeutic rationale for DHA in overcoming therapy resistance caused by cancer stem cells.

overall_design: 1.Global transcriptional profiles of the reprogrammed MMSCs and their parental cells；2.Efect of dihydroartemisinin on the global transcriptional profiles of the reprogrammed MMSCs(U266-CSCs)

first: Yanjun

last: Jia


title: Stromal cells from the murine stomach antrum - single cell RNA seq

summary: The aim of the experiment is to characteirze the non-epithelial cells in the stomach antrum using single cell RNAseg

overall_design: Disccociated cells from murrine stomach antrum were sorted using an antiboby against EPCAM, and EPCAM-negative cells were applied for Sc RNAseq

first: Michael

last: Sigal

first: Sascha

last: Sauer

first: Ramon

last: Vidal


title: Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans

city: Worcester

first: Mohamad

middle: Ali

last: Nasrallah

address: 364 Plantation St

institute: UMass Chan Medical School

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Control of Paneth cell function by HuR regulates gut mucosal growth by altering stem cell activity

city: Baltimore

first: Amol

middle: Carl

last: Shetty

state: Maryland

address: 670 W. Baltimore Street, Floor 3

department: Institute for Genome Sciences

institute: University of Maryland Baltimore

summary: HuR stimulates the activity of intestinal stem cells by enhancing Paneth cell function via activation of mitochondrial metabolism, thus promoting renewal of the intestinal mucosa

overall_design: To obtain cell type-specific transcriptional regulation profiles in the intestinal epithelium after HuR deletion, we performed single-cell RNA-sequencing (scRNA-seq) analysis on the small intestinal mucosa harvested from IE-HuR−/− and control littermate mice. In total, 60,000 high-quality cells were grouped into 18 clusters, which expressed classic cell type markers from the absorptive or secretory lineages, and markers distinctive of ISCs and daughter transient-amplifying cells), following published single-cell transcriptomic signatures in the intestinal epithelium. Secretory cells in the epithelial compartment of the small intestine consisted of PCs, goblet cells, tuft cells, and enteroendocrine cells in both IE-HuR−/− and littermate mice, whereas absorptive cells were marked by various enterocytes. Cell cluster analysis revealed that the numbers of PCs and ISCs decreased in IE-HuR−/− mice compared with control littermate mice, which were consistent with the findings obtained from studies using immunostaining assays.

first: Lan

last: Xiao

first: Jian-Ying

last: Wang


title: circRNA microarray profile  analysis in esophageal squamous cell carcinoma(ESCC) and adjacent normal tissues

first: Yaowen

last: Zhang

summary: The circRNA expression profile related to ESCC in high-incidence areas of China was successfully constructed, and differentially expressed circRNAs were screened out and  their functions were predicted.The circRNA expression in ESCC tissues was significantly different from that in  adjacent normal tissues.GO and Pathway analysis showed that differentially expressed circRNAs were mainly involved in biological functions such as cellular process, metabolic process, biological regulation, binding and catalytic activity, and involved in multiple regulatory pathways including extracellular matrix receptor interaction, adhesion spot, protein digestion and absorption.Then their circRNA-miRNA network was constructed to better understand the related mechanism of circRNAs and provide ideas for exploring the biology functions of circRNAs in ESCC, revealing that the differentially expressed circRNAs were closely related to ESCC.

overall_design: Pairs of ESCC tissues and normal adjacent tissues were selected, and gene chip technology and microarray analysis were used to construct the circRNA expression profile. Differentially expressed circRNAs were screened with FC ≥ 2 times and p < 0.05. The functions of circRNA were predicted by GO and Pathway analysis. The circRNA-miRNA network was constructed to investigate the mechanism of circRNA.

first: Fuyou

last: Zhou


title: Volumetric compression by heterogeneous scaffold embedding promotes cerebral organoid growth and maturation

city: Shen Zhen

first: Shaohua

last: Ma

state: Guangdong Province

address: nanshan street

institute: Tsinghua University

summary: While biochemical regulation has been extensively studied in cerebral organoid modeling protocols, the role of mechano-regulation in directing stem cell fate and organoid development has been relatively unexplored. Volumetric compression, a key aspect of natural brain development, is known to influence neuronal differentiation. However, stiff interpenetrating network compression fails to accurately replicate the dynamic organoid development observed in nature. In this study, we present a novel method of heterogeneous embedding using an alginate-shell-Matrigel-core system. This approach allows for cell-Matrigel remodeling by the inner layer and provides moderate normal compression through the soft alginate outer layer. Our results show significant improvements in cell proliferation and maturation of cerebral organoids, as evidenced by increased expression of neuronal markers such as neurofilament (NF) and microtubule-associated protein 2 (MAP2). Compared to non-alginate embedding and alginate compression groups, volume growth remains unimpeded. Our findings demonstrate the successful mechanical regulation of cerebral organoids, which not only mimics the mechanical environment of brain development but also exhibits a regular growth profile with enhanced maturation. These results highlight the importance and potential practical applications of mechano-regulation in the establishment of brain organoids.

overall_design: Gene expression patterns reflect how cells respond to external stimuli. To examine the effect of alginate compression on organoids, we collected 2 control (without alginate encapsulation) and 3 experimental samples (encapsulated with calcium alginate) for RNA sequencing. RNA isolation and sequencing were performed by BGI Genomics Corporation using the Equalbit RNA BR Assay Kit.

first: Xiaowei

last: Tang

first: Zitian


title: Gene expression in sweet orange infested by Lecanicillium psalliotae

city: kunming

first: xiuyao

last: yang

state: yunnan

address: Southwest Forestry University, 300 Bailong Road, Qingyun Street, Panlong District, Kunming, Yunnan Province, China

institute: Southwest Forestry University

summary: To verify the pathogenicity of Lecanicillium psalliotae invasive pathogens on tsearch  leaves, Lecanicillium psalliotae was identified by isolation and purification. sweet orange leaves were infested with it. The results of the experiments showed that 15 days after Lecanicillium psalliotae infested the leaves of sweet orange, yellow spots grew around the pores and irregular yellow spots appeared on both sides of the leaf veins. This was highly similar to the disease in the field, suggesting that Lecanicillium psalliotae is the causal agent of the yellow spots on sweet orange leaves that cause the leaves to wilt and fall off. In previous studies, Verticillium cutaneum was mainly identified as a biological control agent and a suspected pathogen. In this study, the pathogenicity of Verticillium cutaneum was verified for the first time as a causal agent of leaf spot disease of plants.

overall_design: Sweet orange leaves of uniform size and color, free from mechanical damage, were disinfected on an ultra-clean bench with 4% sodium hypochlorite solution and placed in sterilized petri dishes lined with sterile paper. Then, six small holes were poked on the front of the leaves with a sterile toothpick. In each hole, 3 μl of Lecanicillium psalliotae spore suspension was injected as the treatment group and an equal amount of sterile water was injected as the control group. 3 leaves were set up in both the treatment and control groups. Petri dishes were sealed with sealing film and incubated in the dark at 26°C for 14 days. After the appearance of obvious disease, 2cm of leaves around the sweet orange leaves were collected and stored in liquid nitrogen.

first: Dengxian

last: Xi


title: Butyrate prevents visceral adipose tissue inflammation and metabolic alterations in a mouse model of Friedreich’s ataxia

city: Rome

first: Fabio

last: Zaccaria

address: Via della Ricerca Scientifica 1

country: Italy

institute: University of Rome "Tor Vergata"

summary: Functional enrichment analysis of differentially expressed genes reveals alteration of visceral adipose tissue resembling type 2 diabetes signatures in a mouse model of Friedreich’s ataxia

overall_design: To compare frataxin deficient (KIKO) mice vs. WT, visceral adipose tissue (vWAT)

first: Katia

last: Aquilano

first: Daniele

last: Lettieri Barbato


title: ESC-sEVs rejuvenate aging hippocampal NSCs by transferring SMADs to regulate the MYT1-Egln3-Sirt1 axis

first: zhifeng

last: deng

address: 600 yishan road

institute: shanghai 6th people's hospital

summary: Tissue stem cell senescence leads to stem cell exhaustion, which results in tissue homeostasis imbalance and a decline in regeneration capacity. However, whether neural stem cells (NSCs) senescence occurs and causes neurogenesis reduction during aging is unknown. In this study, mice at different ages were used to detect age-related hippocampal NSCs (H-NSCs) senescence, as well as the function and mechanism of embryonic stem cells derived small extracellular vesicles (ESC-sEVs) in rejuvenating H-NSCs senescence. We found a progressive cognitive impairment, as well as age-related H-NSCs senescence, in mice. ESC-sEVs treatment significantly alleviated H-NSCs senescence, recovered compromised self-renewal and neurogenesis capacities, and reversed cognitive impairment. Transcriptome analysis revealed that Myelin transcription factor 1 (MYT1) is downregulated in senescent H-NSCs but upregulated by ESC-sEV treatment. In addition, knockdown of MYT1 in young H-NSCs accelerated age-related phenotypes and impaired proliferation and differentiation capacities. Mechanistically, ESC-sEVs rejuvenated senescent H-NSCs partly by transferring SMAD4 and SMAD5 to activate MYT1, which downregulated Egln3, followed by activation of HIF2α, NAMPT, and Sirt1 successively. Taken together, our results indicated that H-NSCs senescence caused cellular exhaustion, neurogenesis reduction and cognitive impairment during aging, which can be reversed by ESC-sEVs. Thus, ESC-sEVs may be promising therapeutic candidates for age-related diseases.

overall_design: NSCs mRNA profiles of passage 2, passage 10 treated with pbs, and passage 10 treated with ESC-sEVs

first: Guowen

last: Hu

first: Yuguo

last: Xia

first: Yang

first: Zhifeng

last: Deng


title: MAP3K8 is a major regulator of inflammation in human airway epithelial cells

city: London

first: William

last: Cookson

address: Dovehouse Street

country: United Kingdom

institute: Imperial College London

summary: In this experiment we catalogue temporal variation in transcription occurring during IL1B stimulation under control (non-targeting siRNA control) conditions and partial MAP3K8 siRNA knockdown in the A549 cell line. We measure global gene transcription at 0, 1, 2, 4, 6, 8, and 12 hours using Affymetrix HuGene 1.1 ST array. Nineteen genes demonstrated a distinct temporal response to Il1B stimulation following suppression of MAP3K8.

overall_design: A total of 48 RNA samples derived from the A549 cell line were analyzed as part of this study. The transcriptional response to IL1B stimulation (1 ng/ml IL-1β) was measured at 0, 1, 2, 4, 6, 8, and 12 hours under control and partial MAP3K8 knockdown conditions. A minimum of three replicates were used for each time point-treatment combination.

first: Chih-Yung

last: Chiu

first: Saffron

middle: A

last: Willis-Owen

first: Kenny

last: Wong

first: Stuart

middle: N

last: Farrow

first: Youming

first: Miriam

last: Moffatt

middle: O


title: RNAseq of livers from High Fat Diet and Low Fat Diet fed mice, sampled every 4 hours over one full cycle, living in either short light, long light, or equal light photoperiods

first: Lewin

last: Small

first: Leonidas

last: Lundell

first: Juleen

last: Zierath

middle: B


title: AHR-TFAP2A regulates epidermal differentiation in response to environmental cues [RNA-seq]

city: Nijmegen

first: Jo Huiqing

last: Zhou

address: Geert Grooteplein 26/28

country: Netherlands

institute: Radboud University

summary: The Aryl Hydrocarbon Receptor (AHR) is an environmental sensor and an indispensable regulator of epithelial homeostasis. To investigate AHR-mediated gene regulation, we performed a comprehensive transcriptomic and epigenomic analysis using human primary epidermal keratinocytes. Our results showed that AHR activation led to the induction of canonical transcription factors involved in epidermal differentiation as an early response, i.e. Transcription Factor AP-2α (TFAP2A), while epidermal differentiation-related genes, such as filaggrin and keratins, were activated as late responsive genes. The identified AHR-TFAP2A axis and its role in keratinocyte terminal differentiation was confirmed through AHR and TFAP2A knockout using CRISPR/Cas9. Our findings demonstrate that AHR regulates epidermal differentiation through the transient activation of specific transcription factors, such as TFAP2A, in response to environmental cues. The herein identified AHR-TFAP2A axis provides a promising target for the treatment of diseases related to skin barrier dysfunction.

overall_design: To characterize the gene expression pattern upon AHR activation in keratinocytes, we performed RNA-seq on either TCDD or CT treated keratinocytes. In addition, to identify AHR-responsive enhancers, we performed ChIP-seq of AHR and H3K27ac that marks active enhancers in the genome of keratinocytes after TCDD treatment for 30 and 90 minutes. With integrated analyses of  RNA-seq, AHR, and H3K27ac ChIP-seq data, we identified that TFAP2A is a direct AHR target and is an important transcription factor involved in epidermal differentiation. To further test our hypothesis that AHR controls epidermal differentiation via TFAP2A expression, we knocked down TFAP2A in monolayer primary keratinocyte cultures and performed RNA-seq analysis.

first: Jieqiong

last: Qu

first: Jos

middle: P

last: Smits

first: Felicitas

last: Pardow

first: Noa

last: van den Brink

first: Huiqing

first: Ellen

middle: H

last: van den Bogaard


title: The comparison of gene expression in hematopietic stem cells (HSCs; LSK cells, Lineage-, c-kit+, Sca-1+) from STZ-indued diabetic/nondiabetic mice.

city: Otsu

first: Miwako

last: Katagi

address: seta tukinowa-cho

institute: Shiga university of medical science

summary: To evaluate gene expression of STZ-induced diabetic mice and nondiabetic control mice

overall_design: To evaluate the difference of gene expression between STZ-induced diabetic mice and nondiabetic mice.

first: Hideto

last: Kojima

first: Junko

last: Okano

first: Yuki

last: Nakae

first: Natusko

last: Ohashi

first: Kazunori

last: Fujino

first: Itsuko

last: Miyazawa

first: Takahiko

last: Nakagawa


title: Unravelling the immune signature of herpes zoster: Insights into pathophysiology and the HLA risk profile

city: Antwerp

first: Pieter

last: Meysman

address: Middelheimlaan 1

department: Computer Science

institute: University of Antwerp

summary: The varicella-zoster virus (VZV) infects over 95% of the population and establishes latency afterwards. Reactivation of VZV causes herpes zoster (HZ), commonly known as shingles, which presents as a painful rash in mostly the elderly and people with a weakened immune system. However, HZ might occur in otherwise healthy individuals too. In this study, we have analyzed the immune signature of HZ to better understand HZ’s pathophysiology. We provide a general overview of the antiviral state and the activation of innate and adaptive immune responses during HZ. An extensive exome-wide association study of HZ, incorporating UK Biobank data across white, black and Asian cohorts highlights the MHC locus as a risk factor for HZ development. Therefore, we conducted one of the largest human leukocyte antigen (HLA) association studies on HZ to date (n=138,701 participants) using Fisher’s exact test and identified five protective and four risk HLA alleles associated with the development of HZ. Additionally, differential gene expression and gene ontology analyses revealed upregulation of several genes and host immune pathways during herpes zoster, especially related to type I interferon response but also involved with adaptive immune responses. Intriguingly, no differences in gene expression were noted during convalescence between HZ patients and controls. Our research reveals that HZ susceptibility is largely governed by a complex pattern of variations in the major histocompatibility complex, resulting in modified antigen recognition in HZ patients. Further, we identified key genes and pathways involved in the host immune response to symptomatic VZV reactivation and provided new molecular insights into the development of HZ and its associated risk factors.

overall_design: A total cohort of twenty-six herpes zoster patients aged between 18 and 70 years (median age 51 years; 13 men, 13 women) were prospectively recruited during an active HZ episode, as confirmed by a positive VZV PCR on skin swab or saliva or by significantly elevated (> 4 times) VZV IgG serum titers. Age (± 1 birth year) and sex matched controls without a history of HZ were recruited for each HZ patient and donated blood around the one-year timepoint. To optimize the inclusion of controls, PAXgene RNA of three of the controls was collected during sampling via another study with approval by the Institutional Review Board. Six of the controls also donated a PAXgene RNA tube one year earlier around the same time as blood collection from their matched HZ patients during the active HZ episode, which served as an internal quality control for storage and handling.

first: Romi

last: Vandoren

first: Marlies

last: Boeren

first: Jolien

last: Schippers

first: Esther

last: Bartholomeus

first: Kerry

last: Mullan

first: Nele

last: Michels

first: Olivier

last: Aerts

first: Julie

last: Leysen

first: An

last: Bervoets

first: Julien

last: Lambert

first: Elke

last: Leuridan

first: Johan

last: Wens

first: Karin

last: Peeters

first: Marie-Paule

last: Emonds

first: Hilde

last: Jansens

first: Jean-Laurent

last: Casanova

first: Paul

last: Bastard

first: Arvid

last: Suls

first: Viggo

last: Van Tendeloo

first: Peter

last: Ponsaerts

last: Delputte

first: Benson

last: Ogunjimi

first: Kris

last: Laukens


title: Adapter CAR-T cells to counteract T cell exhaustion and enable flexible targeting in AML

city: Barcelona

first: Lucas

middle: Esteban

last: Wange

address: Dr. Aiguader 88

department: Institut de Biologia Evolutiva

country: Spain

institute: Universitat Pompeu Fabra

summary: Although the landscape for treating acute myeloid leukemia (AML) patients has changed substantially in recent years, the majority of patients will eventually relapse and succumb to their disease. Allogeneic stem cell transplantation provides the best anti-leukemia treatment strategy, but is only suitable in a minority of patients. In contrast to B-cell neoplasias, chimeric antigen receptor (CAR) T-cell therapy in AML has encountered challenges in target antigen heterogeneity, safety, and T-cell dysfunction. We developed a Fab-based adapter CAR (AdCAR) T-cell platform with flexibility of targeting and control of AdCAR T-cell activation. Utilizing AML cell lines and a long-term culture assay for primary AML cells, we were able to demonstrate AML-specific cytotoxicity using anti-CD33, anti-CD123, and anti-CLL1 adapter molecules in vitro and in vivo. Notably, we show for the first time the feasibility of sequential application of adapter molecules of different specificity in primary AML co-cultures. Importantly, utilizing the AML platform, we were able to demonstrate that continuous adapter molecule exposure led to AdCAR T-cell exhaustion through chronic AdCAR stimulation, which was counteracted through treatment-free intervals. As CAR T-cell exhaustion is a well-known cause of resistance, the AdCAR platform might ameliorate CAR T-cell dysfunction.

overall_design: Adapter CAR T-cells of three healthy donors stimulated continuously with anti-CD33 adapter molecule or with a treatment-free interval (TFI) from day 7-14 were sorted and analyzed. Samples: Continuously stimulated = day 0, 14, 21; TFI-stimulated = day 14, 21.

first: Daniel

last: Nixdorf

first: Marion

last: Subklewe


title: m6A methylation regulates hypoxia-induced pancreatic cancer glycolytic metabolism through ALKBH5-HDAC4-HIF1α positive feedback loop

city: Jinan

first: Liu

last: Xiaoyan

address: 247 Beiyuan Street,

institute: The Second Hospital of Shandong University

summary: To study the effects of hypoxia-related m6A modification which were mediated by ALKBH5 in pancreatic cancer, we established  the ALKBH5 knockdown cell lines in PANC-1 cells. And then, the ALKBH5 knockdown cell lines were cultured under hypoxia for 48 h.

overall_design: Comparative gene expression profiling of RNA-seq data from ALKBH5 knockdown cells versus control  cells.

first: Xiaoyan

last: Liu

first: Maoxiao

last: Feng

first: Lutao

last: Du

first: Chuanxin

last: Wang


title: CD4 T cells in Giant Cell Arteritis (scRNA-Seq)

city: Rochester

first: Yuki

last: Sato

state: MN

address: 200 1st ST SW

department: Rheumatology

institute: Mayo Clinic

summary: CD4 T cells are important in GCA

overall_design: Human CD4 T cells from humanized vasculitis mouse model

first: Abhinav

last: Jain

first: Cornelia

middle: M

last: Weyand


title: CD4 T cells in Giant Cell Arteritis


title: Effect of 35d and curcumin treatment on gene expression in GR6 cells

city: Taichung

first: Pei-Chih

last: Lee

address: No. 91, Hsueh-Shih Road

department: Graduate Institute of Biomedical Science

country: Taiwan

institute: China Medical University

summary: To investigate gene expression changes by 35d and curcumin, we treated 1 uM 35d and curcumin for 24h in GR6 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of untreated and treated cells

overall_design: Comparative gene expression profiling analysis of RNA-seq data for untreated cells and 35d or curcumin treated cells.


title: Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [RNA-Seq]

first: Mohamad

last: Nasrallah

state: MA

summary: Sphingolipids are required for diverse biological functions and are degraded by specific catabolic enzymes. However, the mechanisms that regulate sphingolipid catabolism are not known. Here we characterize a transcriptional axis that regulates sphingolipid breakdown to control resistance against bacterial infection. From an RNAi screen for transcriptional regulators of pathogen resistance in the nematode C. elegans, we identified the nuclear hormone receptor nhr-66, a ligand-gated transcription factor homologous to human hepatocyte nuclear factor 4. Tandem chromatin immunoprecipitation-sequencing (ChIP-seq) and RNA sequencing (RNA-seq) experiments revealed that NHR-66 is a transcriptional repressor, which directly targets sphingolipid catabolism genes. Transcriptional de-repression of two sphingolipid catabolic enzymes in nhr-66 loss-of-function mutants drives the breakdown of sphingolipids, which enhances host susceptibility to infection with the bacterial pathogen Pseudomonas aeruginosa. These data define transcriptional control of sphingolipid catabolism in the regulation of cellular sphingolipids, a process that is necessary for pathogen resistance.

overall_design: RNA-seq of C. elegans wild-type (N2) and nhr-66(ok940) animals

first: Nicholas

middle: D

last: Peterson

first: Read

last: Pukkila-Worley


title: Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [ChIP-Seq]

overall_design: DNA binding profile of NHR-66 in C. elegans animals


title: Irisin reduces Amyloid-β by inducing the release of neprilysin from astrocytes following downregulation of ERK-STAT3 signaling

city: Charlestown

first: Joseph

last: Park

address: 114 16th Street

department: Neurology

institute: Massachusetts General Hospital/Harvard Medical School

summary: A pathological hallmark of Alzheimer’s disease (AD) is the deposition of amyloid-β protein (Aβ) in the brain. Physical exercise has been shown to reduce Aβ burden in various AD mouse models, but the underlying mechanisms have not been elucidated. Irisin, an exercise-induced hormone, is the secreted form of fibronectin-domain III containing 5 (FNDC5). Here, using a three-dimensional (3D) cell culture model of AD, we show that irisin significantly reduces Aβ pathology by increasing astrocytic release of the Aβ-degrading enzyme neprilysin (NEP). This is mediated by downregulation of ERK-STAT3 signaling. Finally, we show that integrin αV/β5 acts as the irisin receptor on astrocytes required for irisin-induced release of astrocytic NEP, leading to clearance of Aβ. Our findings reveal for the first time a cellular and molecular mechanism by which exercise-induced irisin attenuates Aβ pathology, suggesting a new target pathway for therapies aimed at the prevention and treatment of AD

overall_design: To compare transcriptional differences in a cell type specific manner, we performed single cell RNAseq based on the conditions below; AD + PBS + IgG; AD + irisin + IgG; AD + irisin + integrin aV/b5 antibody.

first: Dmitry

last: Prokopenko

first: Younjung

last: Choi

first: Eunhee

last: Kim

first: Se Hoon

first: Rudolph

last: Tanzi