title: Gene expression data from 83 cell line with overexpression of ApoD

city: Chengdu

first: Juan

last: Wu

state: Sichuan

address: No. 37 Guo Xue Alley, Wuhou District

department: Anesthesiology

institute: West China Hospital of Sichuan University

summary:
Background: Perineural invasion (PNI) is a prevalent phenomenon in salivary adenoid cystic carcinoma (SACC). Nevertheless, the regulatory mechanism of PNI is largely elusive.
Methods: We detected Apolipoprotein D (ApoD) expression and further determined its role in SACC progression. Subsequently, the contributions of SACC-derived ApoD on neurite outgrowth of dorsal root ganglions (DRGs) cells were explored. Moreover, a series of in vivo assays were conducted to elucidate the role of ApoD in the SACC PNI process.
Results: We observed a dramatic up-regulation of ApoD in the SACC associated with an enhancement of PNI in patient biopsies. We found that SACC-derived ApoD elevated cancer cell migration and invasion. In addition, ApoD could facilitate the neurite outgrowth of cultured DRG cells in a CXCR4-dependent manner in vitro, as well as innervation, angiogenesis, and invasion along peripheral nerves of SACC in vivo. More importantly, by advanced bioinformatic analysis, we unexpectedly revealed a novel phenomenon “tumor cell to neuron-like cell transition” in the ApoD-rich microenvironment in vivo, contributing to the neurogenesis in the SACC tumor.
Conclusion: we discovered a novel role of cancer-derived ApoD in the pathogenesis of PNI, which may represent an effective therapeutic target for SACC in clinics.

overall_design: We performed Transcriptome sequencing of 83 cell line, a SACC cell, with overexpression of ApoD


title: Transcriptional profiling of striatum from a mouse model of Huntington's disease (Q140) crossed with Ccdc82 heterozygous and homozygous mice [Ccdc82]

status: Public on Feb 10 2025

city: Princeton

first: Jeff

last: Aaronson

state: New Jersey

address: 155 Village Boulevard, Suite 200

department: Discovery & Systems Biology

country: USA

institute: CHDI

type: Expression profiling by high throughput sequencing

summary: Striatum was isolated from 6-month-old Ccdc82+/- and Ccdc82-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Q140, Ccdc82+/-, Q140 X Ccdc82+/-, Ccdc82-/-, and Q140 X Ccdc82-/-, 7-8 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the striatum tissues of 6-month-old wild type, Q140, Ccdc82+/-, Q140 X Ccdc82+/-, Ccdc82-/-, and Q140 X Ccdc82-/- mice. N = 7-8 per group.

first: X

middle: W

last: Yang

first: Jim

last: Rosinski


title: Transcriptional profiling of striatum from a mouse model of Huntington's disease (Q140) crossed with Msh3 heterozygous and homozygous mice [Msh3 snRNA-seq]

summary: Striatum was isolated from 12-month-old Msh3+/- and Msh3-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (snRNASeq) was performed on 6 genotypes: WT, Q140, Msh3+/-, Q140 X Msh3+/-, Msh3-/-, and Q140 X Msh3-/-, 4 replicates per genotype.

overall_design: snRNASeq analysis was performed on samples from the striatum tissues of 12-month-old wild type, Q140, Msh3+/-, Q140 X Msh3+/-, Msh3-/-, and Q140 X Msh3-/- mice. N = 4 per group (2M/2F).


title: miR-409-3p and miR-431-5p are key regulators of renal mineralocorticoid receptor expression during the neoatal period [miRNA-seq]

city: Le Kremlin-Bicêtre

first: Say

last: Viengchareun

state: Val de Marne

address: 63 rue gabriel peri

country: France

type: Non-coding RNA profiling by high throughput sequencing

summary: Aldosterone controls sodium homeostasis by binding to the Mineralocorticoid Receptor (MR). We previously identified a specific temporal window during renal development when MR expression is low, explaining the physiological sodium losses observed in newborns at birth. However, underlying molecular mechanisms controlling MR expression remain unknown. Recently, we demonstrated in adult renal KC3AC1 cell line that MR expression is controlled by microRNAs (miR-30c-2-3p and miR-324-5p) in response to tonicity. Herein, we highlight the involvement of two  microRNAs (miR-409-3p and miR-431-5p) in the regulation of MR expression during the neonatal period. RT-qPCR validated candidates microRNAs identified by high throughput screening approach and transfection of a luciferase reporter construct together with miRNAs Mimics or Inhibitors demonstrated their functional interaction with target transcripts. Underexpression strategies using Inhibitors revealed the impact on MR expression and signaling in primary culture renal cells. miR-409-3p and miR-431-5p are increased at D0 in mirror to MR expression. These miRNAs directly affect Nr3c2 (MR) transcript stability and enhances MR expression and signaling at D0. Whereas, overexpression strategies using Mimics, destabilize MR expression and mineralocorticoid signaling in primary culture renal cells at D8. We also confirm that their expression is increased in urine from neonates at birth, an expression that gradually decreased after birth (PREMALDO cohort). Finally, we performed an RNA sequencing to evaluate an integrative network of miRNAs and mRNA differentially expressed between D0 and D8. Differentially expressed genes (DEG) were crossed with the two candidate miRNAs, and 83 differentially expressed target genes (DETG) were obtained. Functional annotation suggested that kidney development and sodium transport/homeostasis pathways were significantly enriched. Our findings provide new predictive and non-invasive biomarkers of renal maturity and mineralocorticoid signaling expression and efficacy in human premature infants.

overall_design: We performed a miRNA-Seq of mouse kidneys harvested at D0 and D8 to identify miRNAs differentially expressed during the neonatal period (D0 and D8) and potentially implicated in the regulation of MR expression


title: Transcriptional profiling of cortex from a mouse model of Huntington's disease (Q140) crossed with Ccdc82 heterozygous and homozygous mice [Ccdc82]

summary: Cortex was isolated from 6-month-old Ccdc82+/- and Ccdc82-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Q140, Ccdc82+/-, Q140 X Ccdc82+/-, Ccdc82-/-, and Q140 X Ccdc82-/-, 7-8 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the cortex tissues of 6-month-old wild type, Q140, Ccdc82+/-, Q140 X Ccdc82+/-, Ccdc82-/-, and Q140 X Ccdc82-/- mice. N = 7-8 per group.


title: Transcriptional profiling of striatum from a mouse model of Huntington's disease (Q140) crossed with Pms2 heterozygous and homozygous mice [Pms2_striatum]

summary: Striatum was isolated from 6-month-old Pms2+/- and Pms2-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Q140, Pms2+/-, Q140 X Pms2+/-, Pms2-/-, and Q140 X Pms2-/-, 6-12 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the striatum tissues of 6-month-old wild type, Q140, Pms2+/-, Q140 X Pms2+/-, Pms2-/-, and Q140 X Pms2-/- mice. N = 6-12 per group.


title: Single cell RNA sequencing analysis of the center, edge and non-wounded regions of healing skin on day 11 post-wounding in wild type mice

city: Baltimore

first: Sam

last: Lee

state: MD

address: 1550 Orleans Street

institute: Johns Hopkins University School of Medicine

summary: We applied single-cell RNA sequencing to investigate specific type of cell populations and their gene expressions on the day of wound closure (post-wounding day 11-12) at the center and edge of the re-epithelialized mouse wound site (1 cm² of whole skin was removed, with samples pooled from 10 mice). Skin samples from non-wounded area were collected as control.

overall_design: Viable cells from the single-cell suspension were selected by sorting, and a single-cell library was prepared using 10x Genomics and sequenced with the Illumina NovaSeq 6000. Downstream bioinformatic analysis of single-cell RNA sequencing data was performed using the Seurat package in R. Cell clusters were annotated according to their identity using specific marker genes.

middle: S


title: Transcriptional profiling of striatum from a mouse model of Huntington's disease (Q140) crossed with Msh3 heterozygous and homozygous mice [Msh3_striatum_6m]

summary: Striatum was isolated from 6-month-old Msh3+/- and Msh3-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Q140, Msh3+/-, Q140 X Msh3+/-, Msh3-/-, and Q140 X Msh3-/-, 7-8 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the striatum tissues of 6-month-old wild type, Q140, Msh3+/-, Q140 X Msh3+/-, Msh3-/-, and Q140 X Msh3-/-, and wild-type mice. N = 7-8 per group.


title: Transcriptional profiling of striatum from a mouse model of Huntington's disease (Q140) crossed with Mlh1 heterozygous and homozygous mice [Mlh1_4m]

summary: Striatum was isolated from 4-month-old Mlh1+/- and Mlh1-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Q140, Mlh1+/-, Q140 X Mlh1+/-, Mlh1-/-, and Q140I X Mlh1-/-, 7-9 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the striatum tissues of 4-month-old wild type, Q140, Mlh1+/-, Q140 X Mlh1+/-, Mlh1-/-, and Q140I X Mlh1-/- mice. N = 7-9 per group.


title: Dopaminylation of triosephosphate isomerase 1 (TPI1) in the endothelial niche bypasses ferroptosis to promote lung regeneration over fibrosis

city: ChengDu

first: Bi-Sen

last: Ding

address: Xinchuan Road

department: State Key Laboratory of Biotherapy

country: China

institute: Sichuan University

summary: Pneumonectomy, resection of left lung lobe, trigger a series of regenerative responses characterized by a multitude of genetic alterations. To investigate the changes in gene expression profiles, we conduct a comparative analysis of various lung cell types isolated from both wildtype mice and genetically mice following pneumonectomy.

overall_design: The experiments conducted a comparative analysis of gene expression changes across different lung cell types in mice of diverse genotypes, with samples collected at various times following pneumonectomy.

first: Chunheng

last: Mo

first: Shiyu

last: Xu


title: Transcriptional profiling of cortex from a mouse model of Huntington's disease (Q140) crossed with Pms2 heterozygous and homozygous mice [Pms2]

summary: Cortex was isolated from 6-month-old Pms2+/- and Pms2-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Q140, Pms2+/-, Q140 X Pms2+/-, Pms2-/-, and Q140 X Pms2-/-, 8 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the cortex tissues of 6-month-old wild type, Q140, Pms2+/-, Q140 X Pms2+/-, Pms2-/-, and Q140 X Pms2-/- mice. N = 8 per group (4F/4M).


title: BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (human)

city: Shanghai

first: Miao

middle: miao

last: Liu

address: Kongjiang Road

institute: liumiaobiotech

summary: Retinal pathological angiogenesis (PA) is a common hallmark in proliferative retinopathies, including age-related macular degeneration (AMD), proliferative diabetic retinopathy (PDR), and retinopathy of prematurity (ROP). The mechanisms underlying PA is complex and incompletely understood. Using oxygen-induced retinopathy (OIR) mouse as a model, the role of extracellular matrix (ECM) protein biglycan (BGN) in PA was studied. Significant upregulation of BGN in the retina of OIR mice and in neovascular proliferative membranes of PDR patients was found. The reduction of BGN expression by Bgn-specific small interfering RNA (siRNA) effectively diminished retinal PA in OIR mouse. Subsequent analysis of the mouse OIR retinal single-cell RNA sequencing data from the Gene Expression Omnibus dataset (GSE150703) suggested pericyte as a source of BGN. This was verified using cultured retinal capillary pericytes. BGN expression in pericytes was highly sensitive to hypoxic stimulation. BGN stimulated retinal PA via the upregulation of C-X-C motif chemokine ligand 12 (CXCL12). Inhibition of the CXCL12-CXCR4 axis effectively diminished PA in OIR mouse. In conclusion, this study demonstrated the stimulatory role of BGN in retinal PA, identified the link between BGN and CXCL12 expression, and further highlighted the role of pericytes in retinal PA.

overall_design: To investigate the role of pericyte-derived BGN in the retinal PA, the gene expression changes of HRMVPCs treated with BGN-specific siRNA or control siRNA under hypoxic conditions for 24 hours was compared.

first: Miaomiao

first: Ping

last: Fei

first: Jia

last: Luo

first: Peiquan

last: Zhao


title: Transcriptional profiling of striatum from a mouse model of Huntington's disease (Q140) crossed with Msh3 heterozygous and homozygous mice [Msh3_striatum]

summary: As part of collaboration between UCLA and CHDI, UCLA is creating knockouts (KOs) of 123 genes, implicated in Huntington’s disease (HD) through various computational modeling efforts. Striatum was isolated from 12-month-old Msh3+/- mice and Msh3-/- (KO) crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Msh3+/-, Msh3-/-, Q140, Q140 X Msh3+/- and Q140 X Msh3-/-, 8 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the striatum tissues of 12-month-old Msh3+/-, Msh3-/-, Q140, Q140 X Msh3+/- and Q140 X Msh3-/-, and wild-type mice. N = 8 per group (4F/4M).


title: BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes

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

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: Gene expression profile at single cell level of hearts of db/+ mice and db/db mice given 1% salt (HFpEF model)

city: Leuven

first: Elizabeth

last: Jones

address: Herestraat 49

department: Cardiovascular Sciences

country: Belgium

institute: KULeuven

summary: Microvascular dysfunction is an important determinant in HFpEF but the role of mural cells herein is still poorly investigated. We aimed to examine the transcriptomic signature of endothelial cells and mural cells of the micro- and macrovascular niche in healthy vs. HFpEF cell RNAsequencing.

overall_design: We prepared a single cell suspension of cardiomyocyte-depleted and CD45+ cells depleted hearts (n=4 male hearts per genotype) and analysed it using single cell RNAsequencing

first: Grootaert

last: Mandy

first: Pasut

last: Alessandra

first: Jones

last: Liz


title: Transcriptional profiling of cerebral cortex from a mouse model of Huntington's disease (Q140) crossed with Msh3 heterozygous and homozygous mice [Msh3_cortex]

first: Jeff

summary: As part of collaboration between UCLA and CHDI, UCLA is creating knockouts (KOs) of 123 genes, implicated in Huntington’s disease (HD) through various computational modeling efforts. Cerebral cortex was isolated from 12-month-old Msh3+/- mice and Msh3-/- (KO) crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Msh3+/-, Msh3-/-, Q140, Q140 X Msh3+/- and Q140 X Msh3-/-, 8 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the cerebral cortex tissues of 12-month-old Msh3+/-, Msh3-/-, Q140, Q140 X Msh3+/- and Q140 X Msh3-/-, and wild-type mice. N = 8 per group (4F/4M).


title: miR-409-3p and miR-431-5p are key regulators of renal mineralocorticoid receptor expression during the neoatal period [RNA-seq]

overall_design: We performed an RNA-Seq of mouse kidneys harvested at D0 and D8 to identify transcripts differentially expressed during the neonatal period and specify their involvement in biological processes and/or signaling pathways.


title: Survival and proliferation of liver stem/progenitor cells by liver endothelial cells

city: Suwon-si

first: Jongsu

last: Kim

address: 2066 Seobu-ro, Jangan-gu, Suwon-si, Gyeonggi-do, Republic of Korea (16419)

country: South Korea

institute: Sungkyunkwan university

summary: Adult liver stem/progenitor cells (LPCs) exhibit robust proliferation upon impaired hepatocyte-mediated liver regeneration. However, the regenerative capacity becomes compromised in chronic liver diseases. Consequently, the promotion of liver regeneration through the utilization of LPCs emerges as a promising alternative therapeutic strategy for patients with chronic liver diseases. LPCs can be massively expanded in vitro as self-renewing organoids, however, lack of the niche cell interactions with LPCs is a major limitation. In this study, we highlight the role of liver endothelial cells (LiECs), as a part of LPC niche cells, in supporting the hepatobiliary organoids (HOs) in long-term culture even in the absence of key growth factors, such as Wnt agonists. Furthermore, LiECs altered the gene expression profile of HOs involved in inflammation, migration, extracellular matrix organization, and receptor signaling pathway through paracrine factors. Our findings expand the role of LiECs for regulating stemness of LPCs and provide a new organoid co-culture model using reduced growth medium.

overall_design: To investigate the signaling pathways in survival and proliferation of liver stem/progenitor cells by liver endothelial cells in 3D organoid culture model, we established hepatobiliary organoids co-cultured with liver endothelial cells. We isolated RNAs from hepatobiliary organoids co-cultured with or without liver endothelial cells, then perfored gene expression profiling analysis.

first: Hyun-Soo

last: Roh

first: Da-Eun

first: Gahee

first: Dengxia

last: Fan

first: HongSook

first: Yong-Hee

first: Jae-Hee

first: ByungGak

first: Kwan-Hyuck

last: Baek

first: DongHa

last: Bhang


title: Transcriptional profiling of striatum and cortex from a mouse model of Huntington's disease (Q140) crossed with Rgs9 heterozygous mice and Msh2 knockout mice [Msh2_6mon]

last: Aaronson

summary: As part of collaboration between UCLA and CHDI, UCLA is creating knockouts (KOs) of 123 genes, implicated in Huntington’s disease (HD) through various computational modeling efforts. Striatum and cortex were isolated from 6-month-old Msh2-/- (KO) mice crossed with the Rgs9+/- and Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 4 genotypes: WT, Het (Q140) KI X Rgs9+/-, Q140, and Het (Q140) KI X Rgs9+/- X Msh2-/-, 8 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the striatum and cortex tissues of 6-month-old Het (Q140) KI X Rgs9+/- X Msh2-/-, Q140 KI, Het (Q140) KI X Rgs9+/-, and wild-type mice. N = 8 per group (4F/4M).

first: Jim

last: Rosinski


title: Genomic profiling of striatum from a mouse model of Huntington's disease (Q140) crossed with Msh3 knockout mice [ATACSeq]

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Striatum was isolated from 12-month-old Msh3-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Genomic analysis (ATACseq) was performed on 4 genotypes: WT, Msh3-/-, Het (Q140) KI, and Het (Q140) KI X Msh3-/-, 6 replicates per genotype.

overall_design: ATACseq analysis was performed on samples from the striatal tissue of 12-month-old Msh3-/-, Het(Q140) KI, Het (Q140) KI X Msh3 -/-, and Wild type mice. N = 6 per group (3F/3M).

first: X

last: Yang


title: Sleep need driven oscillation of glutamatergic synaptic phenotype

city: Dallas

first: Genevieve

last: Konopka

state: Texas

address: 5323 Harry Hines Blvd.

department: Neuroscience

institute: University of Texas Southwestern Medical Center

summary: The response to sleep loss, induced by experimental sleep deprivation (SD), provides insight into the function of sleep. Earlier observations have shown an overall increase in synaptic strength and number of cortical, glutamate, AMPA receptor (AMPAR) synapses in response to SD that is recovered by sleep. However, other aspects of glutamatergic transmission, including NMDA receptor mediated neurotransmission and related upstream synaptic regulators of the glutamate synapse function, have not been well examined. Following SD, we report increased AMPA/NMDA ratio in whole cell recordings of frontal cortical (FC) pyramidal neurons of layers 2-3. Additionally, the ratio of silent/active synapse is decreased after SD reflecting decreased silent synapses and plastic potential to convert silent NMDA to active AMPA synapses. All aspects recover with sleep and are associated with differentially expressed genes (DEGs) affecting glutamatergic synaptic phenotype. The DEGs are enriched for a functional group of synaptic shaping cellular components (SSCs) controling glutamate synapse phenotype, overlap with autism risk genes and are primarily observed in a subtype of excitatory pyramidal neurons that project intra-telencephalically (ExIT neurons). Upstream, sleep-related control is suggested by significant enrichment of genes controlled by transcription factor, MEF2c and nuclear HDAC4, a repressor of MEF2c transcriptional activation. Taken together, we propose a functional role of sleep/wake in FC controlling gene expression, regulating an oscillation of glutamate-synaptic phenotypes that facilitates motor learning and training, and if dysfunctional, increases risk for autism.

overall_design: single nuclei RNA-seq on mice with ad-lib sleep and upon sleep deprivation

first: Kaspar

last: Vogt

first: Ashwinikumar

last: Kulkarni

first: Richa

last: Pandey

first: Mantre

last: Dehnad

first: Robert

last: Greene


title: Effect of all-trans retinoic acid on the transcriptome of naïve and IL4-activated macrophages

city: Urbana

first: Jaume

last: Amengual

state: IL

address: 905 S Goodwin Ave

department: Food Science and Human Nutrition

institute: University of Illinois at Urbana Champaign

summary: To investigate the regulatory role of retinoic acid on the macrophages transcriptome depending on their activation status, we treated naïve or IL4-stimulated murine bone marrow-drived macrophages with retinoic acid or vehicle (DMSO) for 6h

overall_design: Comparative gene expression profiling analysis of RNA-seq data for IL4-stimulated and naïve macrophages exposed to 1µM all-trans retinoic acid for 6 hours

first: Ivan

last: Pinos

first: Jianshi

last: Yu

first: Nageswara

last: Pilli

first: Maureen

middle: K

last: Kane


title: A study on the effect of HIE treatment by umbilical cord blood and EPO using mouse microarray

city: Seongnam-si

first: KyuBum

last: Kwack

address: CHA BioComplex 335, Pangy-ro, Bundang-gu

department: BioMedical Science

institute: CHA University

summary: Neonatal hypoxic–ischemic encephalopathy (HIE) results in neurological impairments; cell-based therapy has been suggested as a therapeutic avenue. Previous research has demonstrated the synergistically potentiated therapeutic efficacy of human umbilical cord blood (UCB) by combining recombinant human erythropoietin (EPO) treatment for recovery from HIE. However, its molecular mechanism is not entirely understood. In the present study, we analyzed the mechanisms underlying the effect of combination treatment with EPO and UCB by transcriptomic analysis, followed by gene enrichment analysis. The HIE model of the neonate was prepared and randomly divided into five groups: sham, HIE, and UCB, EPO, and UCB+EPO treatments after HIE. A total of 376 genes were differentially expressed when |log2FC| ≥ 1-fold change expression values were considered to be differentially expressed between UCB+EPO and HIE. Further assessment through qRT-PCR and gene enrichment analysis confirmed the expression and correlation of its potential target Gene N as an essential gene involved in the synergistic effect of the UCB+EPO combination.

overall_design: At 7 days post-injury, the operated pups were randomly assigned into 5 groups (each group, n=8 to 10). UCB (3 ×10^7 /kg, intraperitoneal injection once at 7d post-injury), EPO (500 IU/kg, intraperitoneal injection for five consecutive days from 7d HIE), UCB+EPO (at the same dose and schedule as the other groups) were intraperitoneally administered, and PBS (five consecutive days from 7 d HIE) was injected as a control (HIE). Five array data were obtained for a total of five samples, one each. A total of 5 samples were named 1) sham, 2) HIE, 3) HIE+EPO, 4) HIE+UCB, and 5) HIE+EPO+UCB according to the treatment method.

first: Joo-Wan

last: Choi

first: Su

middle: J

last: Kang

first: Jee

middle: I

first: MinYoung

last: Kim


title: Integrated transcriptomic and in silico drug screening identifies potential stroma-targeting therapeutics in pancreatic cancer

city: Bellinzona

first: Luciano

last: Cascione

state: Ticino

address: Via Chiesa 5

department: Lymphoma & Genomics Research Program

country: Switzerland

institute: IOR

summary: This study identifies a gene panel that can distinguish two stromal subgroups of resected pancreatic cancers which have different microenvironment features and prognosis, and can be targeted by different therapeutic approaches. In-silico and in-vitro analysis indicates that our proposed signature could be further investigated as a predictor of response of immunomodulatory agents, including anti CD40 therapeutics

overall_design: A custom Nanostring-panel including probes for 198 genes associated to stromal activation was run in the tumour tissue of fully clinically-annotated human resected PDACs (N=48).

first: Chiara

last: Braconi

first: Raffaella

last: Casolino


title: Transcriptional profiling of cortex from a mouse model of Huntington's disease (Q140) crossed with Msh3 heterozygous and homozygous mice [Msh3_cortex_6m]

first: Jeff

last: Aaronson

summary: Cortex was isolated from 6-month-old Msh3+/- and Msh3-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Q140, Msh3+/-, Q140 X Msh3+/-, Msh3-/-, and Q140 X Msh3-/-, 7-9 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the cortex tissues of 6-month-old wild type, Q140, Msh3+/-, Q140 X Msh3+/-, Msh3-/-, and Q140 X Msh3-/- mice. N = 7-9 per group.

first: X

last: Yang

first: Jim

last: Rosinski


title: Transcriptional profiling of cortex from a mouse model of Huntington's disease (Q140) crossed with Mlh1 heterozygous and homozygous mice [Mlh1_4m]

summary: Cortex was isolated from 4-month-old Mlh1+/- and Mlh1-/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 6 genotypes: WT, Q140, Mlh1+/-, Q140 X Mlh1+/-, Mlh1-/-, and Q140I X Mlh1-/-, 7-9 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the cortex tissues of 4-month-old wild type, Q140, Mlh1+/-, Q140 X Mlh1+/-, Mlh1-/-, and Q140I X Mlh1-/- mice. N = 7-9 per group.


title: Nip and ctb3 mutant RNA-seq under CS-PT treatment for 1 day

status: Public on Feb 09 2025

city: Beijing

first: Li

last: Jin

address: College of Agronomy and Biotechnology, China Agricultural University, 100193, China

country: Netherlands

institute: China Agricultural University

summary: To identify the downstream genes regulated by CTB3, we collected panicles from the CTB3-cr1 and Nip plants after 1 day of CS-PT treatment and performed RNA sequencing (RNA-seq). We identified 1020 differentially expressed genes (DEGs), including 810 downregulated genes and 210 upregulated genes. GO enrichment analysis of DEGs identified several highly significant terms in biological processes and in molecular functions. We focused on GO terms related to energy supply and carbohydrate (sugar) metabolism.

overall_design: RNA-seq profiling of panicles from wildtype Nip  (Nip) and CTB3 knockdown mutants (CTB3-cr1) at 1day of CS-PT cold treatment.

first: Jin

last: Li


title: Whole Micro-RNA transcriptome profiling of relapsed /refractory and remission Diffuse Large B cell Lymphoma cases to identify differentially expressed micro RNA

city: CHANDIGARH

first: ashim

last: das

state: pgimer post office

address: research block A, pgimer, pgimer

country: India

institute: pgimer

summary:
Purpose: high throughput sequencing technique has revolutionalized research. The aim is to compare the mi-RNA transcriptome expression between Diffuse Large B cell Lymphoma patients who are in complete remission to those who had relpase or were refractory to first line treatment
Methods-mi-RNA profiles of primary biopsies of complete remission(n=3) and refractory(n=3)/relapsed(n= 4) diffuse large b cell lymphoma cases were generated, using S5 Ion Torrent. The sequencing reads that passed quality filters were analyzed for differential micro-RNA expression in refractory/relapsed cohort using DESeq2. qRT–PCR validation was performed using SYBR Green assays.
Results- we analysed  1.5 million reads mapped to human genome (hg19) per sample, two samples had less than threshold reads reads but micro-RNA having > 10 counts in the same cohort was selected .Reads less than 17 bp were removed using Fastx, then aligned to reference genome hg19 using Bowtie. Differentially expressing micro-RNA in the non responder cohort compared to complete response was found by Dseq . Altered micro-RNA with fold change ≥2.0 and p value 0.001 was selected. Downregulation of three shortlisted mi-RNA was validated with q-RT-PCR.
Conclusions: Our study represents the first detailed analysis of retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

overall_design: micro-RNA transcriptome profile of primary biopsies of complete remission and refractory/relapsed Diffuse Large B cell Lymphoma


title: Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [RNA-seq]

first: Xuefei

last: Guo

state: Bejing

address: Xueyuan road, haidian district

department: Institute of Systems Biomedicine

institute: Peking university health science center

summary: Pancreatic cancer is projected to become the second leading cause of cancer-related deaths globally by 2030, yet effective therapeutic options remain limited. Within the pancreatic cancer tumor microenvironment (TME), tumor-associated macrophages (TAMs) secrete interleukin-1 beta (IL-1β), promoting cancer progression while suppressing type I interferons (IFN-I), which is critical for effective tumor treatment. Utilizing the convolutional neural network (CNN)-based DLINP model developed in our laboratory, we identified Co68—an effective metal catalyst featuring a Phosphine-Nitrogen-Phosphine (PNP)-chelated CoCl₂ complex—as a promising candidate to modulate these immune pathways. In preclinical animal models, Co68 demonstrated superior antitumor efficacy compared to the STING agonist DMXAA and showed enhanced therapeutic effects when combined with PD-1 blockade. Single-cell RNA sequencing (scRNA-seq) revealed that Co68 reprograms TAMs to express interferon-stimulated genes (ISGs), attenuates pro-inflammatory cytokine secretion, and disrupts the IL-1β-PGE2 feedback loop, thereby facilitating the recruitment of NK and cytotoxic CD8+ T cells into the TME. Mechanistically, Co68 activates the IFN-I signaling pathway through the TLR4-TRIF-IFN-I axis and weakens inflammation via the TLR4-SYK-STAT1 pathway. Collectively, these findings highlight the therapeutic potential of Co68, derived from PNP-pincer chemistry, to reshape immune dynamics within the pancreatic cancer TME, positioning it as a promising candidate for innovative immunotherapy strategies.

overall_design: To investigate the transcriptomic mechanisms by which Co68 modulates the inflammatory response induced by lipopolysaccharide (LPS) in macrophages, we performed bulk RNA sequencing (RNA-seq) on the RAW 264.7 cell line. In detail, we conducted a comprehensive gene expression profiling analysis utilizing RNA-seq data from wild-type (WT) RAW 264.7 cells treated with DMSO, LPS, LPS-Co68, and Co68 for a duration of 3 hours. Subsequently, we performed a comparative gene expression profiling analysis of the RNA-seq data across the DMSO, LPS, LPS-Co68, and Co68 treatment groups.


title: Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [scRNA-seq]

overall_design: Single-cell RNA sequencing (scRNA-seq) was employed to investigate the anti-tumor mechanisms of Co68 in comparison to DMXAA and a phosphate-buffered saline (PBS) control in a C57BL/6J mouse model of Pan02 pancreatic cancer


title: Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [ATAC-seq]

overall_design: We employed ATAC-seq to investigate the transcriptomic and epigenetic mechanisms underlying Co68's modulation of the LPS-induced inflammatory response in RAW 264.7 macrophages.  The study included DMSO, LPS, LPS-Co68, and Co68 treatment groups.


title: Transcriptional profiling of striatum and cortex from a mouse model of Huntington's disease (Q140) crossed with Polq heterozygous mice [Polq]

summary: As part of collaboration between UCLA and CHDI, UCLA is creating knockouts (KOs) of 123 genes, implicated in Huntington’s disease (HD) through various computational modeling efforts. Striatum and cortex were isolated from 6-month-old Polq+/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 4 genotypes: WT, Polq+/-, Q140, and Q140 X Polq+/-, 8 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the striatum and cortex tissues of 6-month-old Polq+/-, Q140 KI, Q140 X Polq+/-, and wild-type mice. N = 8 per group (4F/4M).


title: METTL3 Deficiency in Macrophage Aggravates Neutrophilic Asthma by Regulating ZBP1-NLRP3 Inflammasome Activation

city: Shenzhen

first: Bingxin

address: No. 1088 Xueyuan Avenue, Nanshan District Shenzhen

institute: Southern University of Science and Technology

summary: N6-methyladenosine (m6A), the most abundant RNA modification, plays the essential role in the immune disorders. Yet, the role of m6A and its master regulator, methyltransferase-like 3 (METTL3) in asthma remain ambiguous. Here, we found that macrophage deficient in METTL3 aggravates the ovalbumin/lipopolysaccharide (OVA/LPS)-induced neutrophilic asthma. Subsequently, we observed that METTL3 deficiency facilitates NLRP3 but not AIM2 and NLRC4-dependent inflammasome activation and IL-1β secretion. Mechanistically, METTL3 deficiency enhanced NLRP3 inflammasome activation were dependent on upregulation of ZBP1 and TRAF1. Lastly, we elucidated that METTL3 negatively regulates ZBP1 expression through m6A modification dependence. In summary, the study unveils the function of m6A in regulating NLRP3 inflammasome activation in macrophage and identifies potential targets in therapeutic intervention of neutrophilic asthma.

overall_design: BMDM cells from Lyz2-Cre-Mettl3fl/fl and Mettl3fl/fl mice were stimulated overnight with LPS (50 ng/ml), and then incubated with nigericin (10 μM) for 1 h or 3 h.

first: Jinong

last: Wang

first: Zi

last: Chen


title: Mycobacterium tuberculosis resisters despite HIV exhibit activated T cells and macrophages in their pulmonary alveoli [scRNA-seq]

city: Montréal

first: Monica

last: Dallmann-Sauer

state: Quebec

address: 1001 Bd Décarie

country: Canada

institute: McGill

summary: Natural resistance to Mycobacterium tuberculosis (Mtb) infection in some people living with HIV (PLWH) is unexplained. We performed single cell RNA-sequencing of bronchoalveolar lavage cells, unstimulated or ex vivo stimulated with Mtb, for 7 PLWH who were Tuberculin skin test (TST) & Interferon Gamma Release Assay (IGRA) positive (called LTBI) and 6 who were persistently TST & IGRA negative (called resisters). Alveolar macrophages (AM) from resisters displayed a stronger baseline M1 phenotype than LTBI AM. Resisters displayed alveolar lymphocytosis (10%-60%), with enrichment of all T cell subpopulations including CD4+ and CD8+ IFNG-expressing cells. Alveolar lymphocytosis was strongly associated with most of the AM transcriptomic features of resisters. In both groups, mycobactericidal granulysin was expressed almost exclusively by a CD8+ T cell subtype that co-expressed granzyme B, perforin and NK cell receptors. These poly-cytotoxic T lymphocytes (CTL) over-expressed activating NK cell receptors and were increased in resisters. Following challenge with Mtb, only a subpopulation of Intraepithelial Lymphocytes (IEL)-like cells in LTBI participants responded with increased transcription of IFNG. AM from resisters responded with stronger TNF signature at 6h post-infection (p.i.) while at 24h p.i. AM from LTBI displayed stronger IFN-γ signature. Conversely, at 24h p.i. only AM from resisters displayed a significant upregulation of MICA transcripts which encode an activating ligand for the CD8+ poly-CTL. These results suggest that CD8+ CTL and AM mediate the resister phenotype in PLWH.

overall_design: Our study was restricted to people living with HIV (PLWH) on long-term anti-retroviral therapy (ART) with no history of tuberculosis (TB) despite long-term exposure to Mycobacterium tuberculosis (Mtb). The 14 participants belonged to two phenotypic groups of equal size: participants classified as “LTBI (latent TB infection)” who tested Interferon Gamma Release Assay (IGRA) positive and displayed a Tuberculin skin test (TST) ≥ 10 mm, and participants coined “resisters” who persistently tested IGRA negative with a TST = 0 mm. Bronchoalveolar lavage (BAL) were collected from these participants and the recovered cells were kept uninfected (MtbNEG) or challenged with Mtb (MtbINF) for approximatly 6h and 24h. Single-cell RNA-sequencing (scRNA-seq) was performed to investigate the BAL cellular composition, gene expression levels in the absence of Mtb and the transcriptomic responses to Mtb challenge. BAL cells from one resister participant were lost due to high proportion of dead cells. CITE-seq was performed in two libraries, one LTBI and one resister, to aid in the cell-type annotation.

first: Vinicius

middle: M

last: Fava

first: Stephanus

middle: T

last: Malherbe

first: Candice

last: MacDonald

first: Marianna

last: Orlova

first: Elouise

middle: E

last: Kroon

first: Aurélie

last: Cobat

first: Stéphanie

last: Boisson-Dupuis

first: Eileen

middle: G

last: Hoal

first: Laurent

last: Abel

first: Marlo

last: Möller

first: Jean-Laurent

last: Casanova

first: Gerhard

last: Walzl

first: Nelita

last: du Plessis

first: Erwin

last: Schurr


title: The landscape of enhancer transcription in prostate cancer [ATAC-Seq]

city: Wuhan

first: Zezhong

last: Xiong

address: 1095 Jiefang Ave. Wuhan, P.R.China

institute: Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology

summary:
Current genome-wide detection of chromatin accessibility uses the assay for transposase-accessible chromatin (ATAC-seq). To a provide panoramic view of the chromatin accessibility landscape in prostate cancer and normal  prostate, we performed ATAC-seq in 20 pairs of prostate cancer tissues and matched adjacent tissues.
Assay of transposase accessible chromatin with high-throughput sequencing (ATAC-seq) for 20 pairs of prostate cancer tissues and matched adjacent tissues.

overall_design: Comparative analysis of ATAC-seq data for prostate cancer tissues and matched adjacent tissues

first: Yue

last: Ge


title: RNA sequencing uncover crucial genes mediating progression of in large-artery atherosclerotic and small-artery occlusion ischemic stroke

city: guangdong

first: wenzhen

last: he

address: 57 Changping Road, Shantou, Guangdong

institute: First Affiliated Hospital of Shantou University Medical College

summary: The goal of our study is to uncover the pathogenesis of large-artery atherosclerotic ischemic stroke (LAAIS) and small-artery occlusion ischemic stroke (SAOIS) and analyze their difference using RNA sequencing.RNA sequencing was used to filtrate differentially expressed mRNAs (DEmRNAs) and lncRNAs (DElncRNAs) in LAAIS and SAOIS. Specific DEmRNAs and DElncRNAs in LAAIS and SAOIS were further foun. Functional annotation and DElncRNA-DEmRNA co-expression network was built to reveal biological function of DEmRNAs.

overall_design: The cohort subjected to RNA-Seq consisted 3 LAAIS patients ， 3 SAOIS patients and 3 healthy individuals.

first: Wenzhen

last: He


title: Transcriptional profiling of striatum and cortex from a mouse model of Huntington's disease (Q140) crossed with Tcerg1 heterozygous mice [Tcerg1]

city: Princeton

first: Jeff

last: Aaronson

address: 155 Village Boulevard, Suite 200

institute: CHDI

summary: As part of collaboration between UCLA and CHDI, UCLA is creating knockouts (KOs) of 123 genes, implicated in Huntington’s disease (HD) through various computational modeling efforts. Striatum and cortex were isolated from 6-month-old Tcerg1+/- mice crossed with the Q140 knock-in (KI) HD mice and their respective controls. Transcriptomic analysis (RNASeq) was performed on 4 genotypes: WT, Tcerg1+/-, Q140, and Q140 X Tcerg1+/-, 8 replicates per genotype.

overall_design: RNASeq analysis was performed on samples from the striatum and cortex tissues of 6-month-old Tcerg1+/-, Q140 KI, Q140 X Tcerg1+/-, and wild-type mice. N = 8 per group (4F/4M).

first: Jim

last: Rosinski


title: Transcriptome-wide characterization of m6A methylation in colorectal cancer

city: Guangzhou

first: Huichuan

last: Yu

state: Guangdong

address: 26 Yuancun Erheng Road

institute: Sun Yat-sen University

type: Methylation profiling by high throughput sequencing

summary: N6-Methyladenosine (m6A) is the most prevalent internal chemical modification of mRNAs in eukaryotes, and m6A methylations are crucial in cancer development. We characterized RNA m6A methylation in colorectal cancer to investigate its association with current molecular phenotyping system.

overall_design: RNA m6A methylation was profiled in the tumor samples and adjacent normal tissue samples collection from colorectal cancer patients by using MeRIP-seq

first: Yanxin

last: Luo


title: Vanguard is a glucose deprivation-responsive long non-coding RNA essential for chromatin remodeling-reliant DNA repair

city: hefei

first: Ben

last: Zhang

state: anhui

address: daoxiangcun

department: Division of Life Sciences and Medicine

institute: University of Science and Technology of China

summary: Glucose metabolism contributes to DNA damage response (DDR) pathways by regulating chromatin remodeling, double-strand break (DSB) repair, and redox homeostasis, although the underlying mechanisms are not fully established. Here, we reveal a previously uncharacterized long noncoding RNA we call Vanguard which acts to promote HMGB1-dependent DNA repair in association with changes in global chromatin accessibility. Vanguard expression is maintained in cancer cells by SP1-dependent transcription according to glucose availability and cellular ATP levels. Vanguard promotes complex formation between HMGB1 and HDAC1, with the resulting deacetylation of HMGB1 serving to maintain its nuclear localization and DSB repair function. However, Vanguard downregulation under glucose limiting conditions promotes HMGB1 translocation from the nucleus, increasing DNA damage and compromising cancer cell growth and viability. Moreover, Vanguard silencing increases the effectiveness of poly (ADP-ribose) polymerase inhibitors (PARPi) against breast cancer cells with wildtype breast cancer gene-1 status, suggesting Vanguard as a potential therapeutic target.

overall_design: sh-ctrl (n=1) compare with sh VNGD (n=1)

first: Pengfei

first: Mian

last: Wu

first: Lianxin

last: Liu


title: Identification of transcription factor combinations that promote axonal sprouting in the injured spinal cord and regeneration-associated gene expression

status: Public on Feb 08 2025

city: Amsterdam

first: Matthew

last: Mason

address: Meibergdreef 47

department: Neuroregeneration

institute: Netherlands Institute for Neuroscience

summary: Axon regeneration after injury to the central nervous system is limited by an inhibitory environment but also because injured neurons fail to initiate expression of regeneration associated genes (RAGs), thought to be required for robust long-distance growth. The potential of strong RAG expression to promote CNS regeneration is exemplified by the conditioning lesion model, whereby peripheral nerve injury promotes regeneration of centrally projecting branches of the injured neurons. RAG expression could potentially be induced by delivery of the right combination of transcription factors (TF), but the specific TFs required remain to be identified. We here begin with a focused bioinformatics approach, analyzing binding site motifs in the promoters of the RAG program to identify nine candidate growth-promoting TFs. In vitro screening then identified two combinations, KLF7/MEF2 and ATF3/KLF7/MEF2, that had potent neurite-growth promoting activity, the latter being the more powerful. We expressed TFs in vivo in L4/L5 dorsal root ganglia to test whether these combinations would promote regeneration and activate the RAG program, mimicking the conditioning lesion effect. KLF7 and MEF2 were also tested individually for comparison. KLF7/MEF2, but not ATF3/KLF7/MEF2 or the individual TFs, promoted axonal sprouting into the lesion site and improved functional recovery. We also generated gene expression profiles of laser dissected dorsal root ganglion neurons specifically expressing these TF combinations, and of DRG neurons that had been axotomized. Unexpectedly, the MEF2-VP16 construct used had little transcriptional activity in vivo, suggesting additional steps may be required to achieve full MEF2 activity. All combinations except MEF2 alone induced RAG expression mirroring that induced by axotomy to significant extents, while ATF3/KLF7/MEF2, KLF7 and ATF3, but not KLF7/MEF2 also induced apoptosis-related genes which may hinder regeneration. In conclusion,  the combination KLF7/MEF2 partially mimics the conditioning lesion effect and promotes functional improvement.

overall_design: All samples are laser-dissected large diameter neurons from rat dorsal root ganglion, following either: adeno-associated viral vector delivery expressing transcription factors with fluorophores, or only fluorophore (control group); or sciatic nerve injury; or from naïve DRG (control group for nerve injury ). The TFs over-expressed in each group were: ATF3, KLF7, MEF2, KLF7/MEF2, ATF3/KLF7/MEF2, no TF (survival time 4 weeks); sciatic nerve injury survival times were 1 day and 7 days. All groups were performed with n=4.

first: Callan

last: Attwell

first: Inés

last: Maldonado-Lasunción

first: Joost

last: Verhaagen


title: SND1-SMARCA5 interaction strengthened by PIM promoted the proliferation, metastasis and chemoresistance of ESCC

city: Luzhou

first: Jian

middle: Yan

address: No. 25, TaiPing Road, JiangYang District, Luzhou, Sichuan

institute: The Affiliated Hospital of Southwest Medical University

summary: Chromatin remodeling plays a pivotal role in the progression of esophageal squamous cell carcinoma (ESCC), yet the precise mechanisms remain poorly understood. Here, we elucidate the critical function of staphylococcal nuclease and tudor domain-containing 1 (SND1) in modulating chromatin dynamics, thereby driving ESCC progression in both in vitro and in vivo models. Our data revealed that SND1 was markedly overexpressed in ESCC cell lines. Silencing SND1 disrupted histone modifications, attenuated RNA polymerase II activity, and precipitated increased chromosomal aberrations and DNA damage, particularly following camptothecin treatment. These molecular perturbations culminated in diminished cellular proliferation, metastasis and chemoresistance. We further identified that the regulatory effects of SND1 on chromatin are mediated through its interaction with SMARCA5, a process potentiated by PIM1-catalyzed phosphorylation of SND1 at serine 426. This SND1-SMARCA5 interaction is essential for the transcriptional activation of CUX1, a key oncogene implicated in ESCC progression. Notably, disruption of SND1S426 phosphorylation impaired the SND1-SMARCA5 interaction, leading to significant inhibition of ESCC tumor growth and metastatic potential in vivo. Our findings unveil a novel mechanistic axis involving SND1 and SMARCA5 in chromatin remodeling and oncogenesis, offering promising therapeutic targets for ESCC intervention.

overall_design: The influence of SND1 on chromatin remodeling in ESCC cell was evaluated by rna interference, western blot, karyotype assay, laser confocal and ATAC-sequence. Colony formation and cell cycle array were used to evaluate cell proliferation. The metastasis and chemoresistance of ESCC cells were studied by transwell, plate survival and flow cytometry respectively. Xenograft mice and liver metastasis model were used to evaluate the proliferation and metastasis of ESCC. The mechanism of SND1 in ESCC was studied through Co-IP, mass spectrometry, ChIP-qPCR, pull down and laser confocal. The correlation of SND1 and its downstream gene with ESCC were investigated through IHC respectively.

first: QunLun

last: Yan

first: Shan

last: Huang

first: Zhi

last: Hu

first: Bin

last: Han


title: Effect of external cues on clock-driven time-of-day specific protection from Influenza A infection

city: Philadelphia

first: Thomas

last: Brooks

address: 3400 Civic Center Blvd

department: ITMAT

institute: University of Pennsylvania

summary: Influenza and other respiratory viral pathogens are leading causes of mortality and morbidity. We have previously shown that circadian rhythms confer temporal protection from influenza infection. Here, we investigate whether the endogenous circadian clocks need optimal cycling of entraining cues to mediate this protection. We used two key entraining factors-- light-dark cycling and meal timing-- to determine their relative importance in allowing the host to benefit from its endogenous circadian rhythms. First, we demonstrate that disrupting environmental lighting cues, within a critical window of vulnerability, abrogated the time-of-day specific protection; this poor outcome is mediated by a dysregulated immune response evidenced by the accumulation of inflammatory monocytes and CD8+ cells in the lungs and transcriptomic profile with an exaggerated immune response. Importantly, rhythmic meal timing mitigated the adverse effects of disrupted light cycles. Our findings highlight the crucial interplay between peripheral and central clocks in shaping influenza outcomes, offering significant translational potential for improving the care of critically ill patients with respiratory viral infections.

overall_design: Specific pathogen-free 8-12 week-old C57bl/6J mice  were placed in circadian cabinets on reverse light-dark cycles. After 4-6 weeks of acclimatization in these cabinets, mice were anesthetized lightly with isoflurane prior to being infected intranasally (i.n.) with mouse-adapted influenza virus (PR8 ). Given the use of circadian cabinets, mice were simultaneously infected at either ZT23 or ZT11 and maintained in 12 hr light-dark cycle. The dose chosen was likely to cause >50% mortality when mice were infected at ZT11. On day four p.i. a subset of ZT23-LD mice were moved to constant light until the end of the study. Lungs were collected at day 8 p.i., at the same ZT as the initial infection, and RNA was extracted.

first: Oindrila

last: Paul

first: Gregory

middle: R

last: Grant

first: Shaon

last: Sengupta


title: CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (YTHDF2-RIPseq)

city: tianjin

first: meixi

last: wang

address: Tianjin Sports Institute North Road Huanhu West Road

institute: Tianjin Medical University Cancer Hospital

summary: As the third most common cause of cancer-related mortality, hepatocellular carcinoma (HCC) is a global health concern. Despite its prevalence, treatment options are limited, underscoring the need to identify potential therapeutic targets and strategies. Here, we identified amplification of CRTC2, situated in the 1q21.3 region, due to copy number alterations in HCC. In a cohort of patients with HCC, CRTC2 protein levels were frequently elevated and correlated with poor prognosis. Genetic depletion of CRTC2 significantly impeded the onset and progression of HCC in mouse models. CRTC2 formed cytoplasmic condensates that recruited the m6A reader YTHDF2. Furthermore, CRTC2 promoted the translocation of m6A-modified mRNAs from decay sites to polyribosomes by interacting with PABP1. The activities of CRTC2 counteracted YTHDF2-mediated mRNA degradation to enhance the translational efficiency of specific mRNAs, including those encoding LRP5 and c-Jun. Targeting CRTC2 in hepatocytes using AAV8.sgCRTC2 elicited substantial therapeutic benefits in HCC mouse model and significantly enhanced the sensitivity to lenvatinib. Together, this research elucidates the pivotal role and underlying molecular mechanisms of CRTC2 in hepatocarcinogenesis and lenvatinib-resistance, highlighting its potential clinical and therapeutic applications.

overall_design: To investigate the cooperative function CRTC2-YTHDF2 co-condensates in N6-methyladenosine modificated mRNA fate transition, RIP-seq for YTHDF2 was applied to identify targets gene in HCCLM3 cells.


title: CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (m6A-seq)

overall_design: To investigate the cooperative function CRTC2-YTHDF2 co-condensates in N6-methyladenosine modificated mRNA fate transition, m6A-seq was used to reveal alterations in m6A methylation patterns in HCCLM3 cells.


title: RNA-sequencing of inguinal white adipose tissue (iWAT) from kynurenine 3-monooxygenase (Kmo) knockout mice and wild-type littermates on chow and high-fat diets.

city: ANN ARBOR

first: Jorge

middle: L

last: Ruas

state: Michigan

address: 2800 Plymouth RD, B025-2681 NCRC - Ruas Lab NCRC B025

institute: University of Michigan

summary: To investigate if chronically elevated circulating kynurenic acid (KYNA) and reduced quinolinic acid (QUIN) levels affect whole-body energy metabolism, we used a knockout-first gene targeting strategy to eliminate Kmo gene expression in mice. We conducted a series of metabolic assessments on male and female mice fed either a chow or high-fat diet (HFD) and performed RNA-sequencing on the inguinal white adipose tissue (iWAT) from male Kmo-defficient mice and their wild-type littermate controls on chow and high-fat diets.

overall_design: RNA sequencing analysis of inguinal white adipose tissue from whole-body male Kmo knockout mice and wild-type littermate controls on chow and high-fat diets (n = 4, age = 6-7 months). Total RNA was extracted using TRI reagent (Sigma-Aldrich, T9424) according to the manufacturer's instructions. RNA was further purified, and DNase treated (Zymo, R1013), and integrity confirmed prior to sequencing (Agilent Technologies, 2100 Bioanalyzer), with an RNA integrity number (RIN) greater than 7 as a threshold. Samples were purified by poly-A enrichment before library preparation using the Illumina NovaSeq X Plus Series platform with a paired-end 150 base pair strategy.

first: Kyle

middle: D

last: Dumont

first: Paulo

last: Jannig


title: Methyltransferase-like 3 mediates m6A modification of heme oxygenase 1 mRNA to induce ferroptosis of renal tubular epithelial cells in acute kidney injury

city: Zhengzhou

first: Linxiao

last: Lv

address: Longhu Central Ring Road No.1

institute: the first affiliated hospital of Zhengzhou university

summary: As an iron-dependent programmed cell death model, ferroptosis has been reported to be involved in the pathogenesis of acute kidney injury. Methyltransferase-like 3 (METTL3) -mediated m6A modification has recently been associated with various renal diseases. However, the relationship between METTL3 and ferroptosis is unclear. In order to further study the molecules involved in that, we first performed m6A sequencing on the kidneys of the control mice and the mice injected with folic acid(FA).

overall_design: MeRIP-seq analysis for control group and FA group(intraperitoneal injection of folic acid) in C57BL mice.

first: Mingyang

first: Sijie

last: Zhou


title: The landscape of enhancer transcription in prostate cancer [RNA-Seq]

first: Zezhong

last: Xiong

summary:
To construct the enhancer transcription expression profile, we performed RNA-seq in 20 pairs of prostate cancer tissues and matched adjacent tissues.
We then performed enhancer transcription expression profiling analysis using data obtained from RNA-seq of 20 pairs of samples.

overall_design: Comparative transcripts expression profiling analysis of RNA-seq data for prostate cancer tissues and matched adjacent tissues

first: Yue

last: Ge


title: Chronic stress promotes intestinal stem cell aging

city: Shanghai

first: Guoying

last: Zhang

address: 320 Yueyang Road

institute: SHANGHAI INSTITUTE OF NUTRITION AND HEALTH. CAS

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

overall_design: Refer to individual Series


title: Chronic stress promotes intestinal stem cell aging [scRNA-seq]

summary:
To elucidate alterations in intestinal cell types under chronic stress, we conducted scRNA-seq analysis of intestinal crypts from NT and ES models. After that, we found that significant changes in ISCs in the ES group compared to the NT group. To validate the functional roles of ISCs, we performed RNA-seq of ISCs under different treatment conditions, we identified Chrm3-dependent differential genes between NT and ES groups, particularly noting downregulated genes associated with stemness and proliferation (e.g., Olfm4, Lgr5, and Mcm4), and upregulated genes linked to aging and calcium signaling pathways (e.g., Cdkn1a, Orai1, and Chp2), which contribute to ISC aging. These findings provided mechanistic insights into targeting these pathways to enhance intestinal function and integrity. Furthermore, to assess the impact of stress-induced changes in microbiota composition on ISC stemness, we synchronized microbiota between NT and ES groups through co-housing conditions and employed 16S rDNA sequencing. This analysis aimed to ascertain the possibility that changes in the microbiota composition whether contribute to the decline in ISC stemness under stress conditions.
scRNA-seq of crypts were used to to characterize the diversity of cell lines under chronic stress. RNA-seq of ISC in Chrm3Lgr5+/+ and Chrm3Lgr5-/- mice from NT and ES mice were taken to delineate altered pathways and the mechanisms underlying ISC changes in ES model. 16S rDNA-seq (available in PRJNA1090629) were employed to confirm microbiota synchronization between NT and ES groups under co-housing conditions.

overall_design: Crypts from wild-type mice in the NT and ES groups were isolated and analyzed using single-cell RNA sequencing (scRNA-seq).

first: Jun

last: Qin


title: Chronic stress promotes intestinal stem cell aging [RNA-seq]

summary:
To elucidate alterations in intestinal cell types under chronic stress, we conducted scRNA-seq analysis of intestinal crypts from NT and ES models. After that, we found that significant changes in ISCs in the ES group compared to the NT group. To validate the functional roles of ISCs, we performed RNA-seq of ISCs under different treatment conditions, we identified Chrm3-dependent differential genes between NT and ES groups, particularly noting downregulated genes associated with stemness and proliferation (e.g., Olfm4, Lgr5, and Mcm4), and upregulated genes linked to aging and calcium signaling pathways (e.g., Cdkn1a, Orai1, and Chp2), which contribute to ISC aging. These findings provided mechanistic insights into targeting these pathways to enhance intestinal function and integrity. Furthermore, to assess the impact of stress-induced changes in microbiota composition on ISC stemness, we synchronized microbiota between NT and ES groups through co-housing conditions and employed 16S rDNA sequencing. This analysis aimed to ascertain the possibility that changes in the microbiota composition whether contribute to the decline in ISC stemness under stress conditions.
scRNA-seq of crypts were used to to characterize the diversity of cell lines under chronic stress. RNA-seq of ISC in Chrm3Lgr5+/+ and Chrm3Lgr5-/- mice from NT and ES mice were taken to delineate altered pathways and the mechanisms underlying ISC changes in ES model. 16S rDNA-seq were employed to confirm microbiota synchronization between NT and ES groups under co-housing conditions.

overall_design: ISCs from Lgr5CreERT2-IRES-GFP; Chrm3flox/flox mice of NT and ES groups with vehicle (Chrm3Lgr5+/+) or TAM (Chrm3Lgr5−/−) injection for 3 days before the ES modeling, and ISCs from Lgr5CreERT2-IRES-GFP mice of young (2month) and old (18month) groups, were isolated by Fluorescence-activated cell sorting (FACS) according to the presence of EGFP signal and analyzed using RNA-Seq.


title: Mechanism of Jingu Zhitong Gel in treatment of knee osteoarthritis based on IL-17 signaling pathway

city: Jiangsu Lianyungang

first: xu

middle: xin

last: yu

state: Lianyun District

address: Jiangning industrial city,Economic and Technological Development Zone

department: Drug screening research department

institute: Jiangsu Kanion Pharmaceutical Co.,Ltd.

summary: In this study, transcriptome sequencing was used to study the mechanism of Jingu Zhitong gel in the treatment of osteoarthritis. We identified the key pathways and key genes for the treatment of KOA by transcriptome sequencing of rat synovial tissue, and completed qPCR validation. The results showed that IL-17 was a targeted pathway in the pathogenesis of osteoarthritis. MMP13, MMP3, cxcl6, CCL17, S100A8, S100A9, Lcn2 and FosB can induce the upregulation of IL-17 signaling pathway, thereby reducing synovial inflammation. This study provides a new idea for the molecular mechanism of Jingu Zhitong gel in the treatment of KOA.

overall_design:
Specific Pathogen-Free (SPF) male SD rats  were randomly divided into control group, model group, Jingu Zhitong Gel high, medium, and low dose groups (1.24, 0.62, 0.31 g/kg), Votalin ointment group (0.105g/kg), and Qingpeng ointment group (0.105 g/kg), with 10 rats in each group. TheKOAmodel of rats was conducted according to the previous literature description[9], 50μL of MIA solution (40 mg/mL) was injected into the lateral side of the patella using an insulin syringe. Rats in the control group were injected with 50μL of sterile physiological saline. The intervention was initiated on day 1 of model establishment and administered twice a day for 14 days.
DESeq2 was used to analyze differentially expressed genes (DEGs)，and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to identify significant pathways. Furthermore, Gene set enrichment analysis (GSEA) was used to identify the key signaling pathways of Jingu Zhitong Gel, and STRING functional protein association network was used to analyze the interaction network, Eight key hub genes of Jingu Zhitong Gel were identified by using the stringapp plugin in Cytoscape.
we performed qPCR experiments on eight key hub genes, confirming the accuracy of the analysis results.

first: Xinyu

last: Xu

first: Zhenzhen

last: Su

first: Jing

last: Liu

first: Weiwei

last: Xing

first: Xinzhuang

first: Liang

last: Cao

first: Zhenzhong

last: Wang

first: Ziyin

last: Wu

first: Wei

last: Xiao


title: Effect of antibiotic-mediated gut microbiota perturbation on postnatal mice ileum transcriptomics

city: Jatani

first: Uday

last: Pandey

address: NISER, Jatani, Odisha

department: Biological Sciences

institute: National Institute of Science Education and research

summary: The postnatal period is one of the important windows for developing the gastrointestinal tract's structure-function and associated mucosal immunity. Recent studies suggest a promising contribution of gut microbiota in maintaining host health, immunity, and gut development. However, the function of postnatal gut microbiota dynamics concerning intestinal mucosal development needs to be better understood. To decipher the causal role of gut microbiota on barrier integrity and intestinal epithelium development, we executed an antibiotic-mediated perturbation and tracked the kinetics in postnatal mice. We observed a postnatal age-related impact of antibiotic-mediated gut microbiota perturbation with a substantial decrease in total bacterial load on P14D and also in the barrier integrity and IECs marker. To enhance our knowledge of the mechanisms behind this, we employed a global transcriptomics approach to see the alterations in the mucosal innate immunity and other relevant pathways.

overall_design: Postnatal mice were orally gavaged with AVNM (Ampicillin, Vancomycin, Neomycin and Metronidazole) cocktail once daily from P3D to P14D along with a set of vehicle control (PBS). Mice were sacrificed at P14D from the two groups (control and AVNM) and collected from different littermates' separate cages to minimize the effect. After sacrifice, the ileum was dissected out, washed with cold PBS, cut into small pieces, and stored in the RNAlater. High-quality RNA was extracted using Direct- zol RNA miniprep (Zymo Research), and quality and quantity were determined using Nanodrop, Gel electrophoresis, Qubit and Tapestation.

first: Pandey

last: Uday

first: Shah

last: Srishti

first: Aich

last: Palok


title: TRMT6-mediated tRNA m1A modification serves as a translational checkpoint of histone biosynthesis and facilitates colorectal cancer progression [Ribo]

first: En-Wei

last: Tao

address: 145 Middle Shandong Road

institute: Shanghai Jiao Tong University

summary: Reprogramming of mRNA translation drives malignant transformation and cancer development. Recently, increasing studies have demonstrated that tRNA modification emerges as a critical regulator of translational reprogramming; however, its function in cancers remains largely elusive. Herein, we identify the oncogenic role of tRNA N1-methyladenosine (m1A) modification in colorectal cancer (CRC). Targeting m1A methyltransferase TRMT6 in CRC cells decreases the abundance of a specific subset of tRNAs (e.g., tRNA-Arg-ACG-1-1, tRNA-Lys-TTT-1-1) and impairs histone mRNA translation in a codon-biased manner, thus restricting histone biosynthesis and cell cycle progression. We further demonstrate that the combination of TRMT6 inhibition and CDK4/6 inhibition shows a stronger anti-cancer effect on CRC cells by synergistically inhibit histone biosynthesis. Collectively, our study reveals that tRNA m1A modification acts as a translational checkpoint of histone biosynthesis and promotes CRC progression, providing new insights for the development of efficient therapeutic strategies against CRC.

overall_design: Comparative ribosome footprinting profiling analysis of RKO cells and its KD derivative (shTRMT6).

first: Ying-Xuan

last: Chen

first: Jing-Yuan

last: Fang

first: Qin-Yan

last: Gao


title: TRMT6-mediated tRNA m1A modification serves as a translational checkpoint of histone biosynthesis and facilitates colorectal cancer progression [RNA]

overall_design: Comparative gene expression profiling analysis of RNA-seq data for RKO cells and its KD derivative (shTRMT6).


title: Endogenous aryl hydrocarbon receptor ligands-dysregulated transcriptomic profiles and vascular function in rat placentas

city: Madison

first: chi

last: zhou

state: WI

address: 202 S. Park Street, PAB1, Meriter Hospital

department: Department of OB/Gyn

institute: University of Wisconsin-Madison

summary: Preeclampsia (PE) is a hypertensive disorder and a leading cause of maternal and fetal mortality and morbidity during human pregnancy. Aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, regulates vascular development and function during pregnancy. Here, we report the important role of endogenous AhR ligands in vascular growth and function during pregnancy using a rat model.  We found that exposure of pregnant rats to an endogenous AhR ligand (ITE, [2-(1’H-indole-3’-carbonyl)-thiazole-4-carboxylic acid methyl ester]) elevated maternal blood pressure and induced proteinuria, while decreased uteroplacental blood flow and fetal/ placental growth, all of which are hallmarks of PE. ITE also dysregulated transcriptomic profiles of rat placentas in a fetal sex-specific manner. The ITE-dysregulated genes were enriched in biological function and pathways highly relevant to diseases of heart, liver, and kidney, vascular function, and inflammation responses. Collectively, we conclude that dysregulation of endogenous AhR ligands may contribute to the PE-impaired vascular function through fetal sex-specific regulation of immune cell infiltration and transcriptomes. These AhR ligand-activated genes and pathways might represent promising therapeutic and sex-specific targets for PE-impaired vascular function.

overall_design: To investigate the role of ITE on placental function. Pregnant rats were treated with ITE.

first: Yingjie

last: Zhao

first: Chi

last: Zhou

first: Sathish

last: Kumar

last: Zheng


title: TRMT6-mediated tRNA m1A modification acts as a translational checkpoint of histone synthesis and facilitates colorectal cancer progression


title: TRMT6-mediated tRNA m1A modification serves as a translational checkpoint of histone biosynthesis and facilitates colorectal cancer progression [tRNA]

overall_design: Comparative tRNA expression profiling analysis of tRNA-seq data for RKO cells and its KD derivative (shTRMT6).


title: SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [CUT&RUN]

city: Cincinnati

first: Richard

last: Lu

state: Ohio

institute: CINCINNATI CHILDREN'S HOSPITAL MEDICAL CENTER

summary: To identify potential direct targets of SUV39H1, we  performed Cut&Run-seq for H3K9me3 and SUV39H1 genomic occupancy

overall_design: Cut&Run for H3K9me3 and Suv39H1 in SU-DIPG13 and SU-DIPG36 cells

first: Dazhuan

last: Xin

first: Yunfei

last: Liao


title: SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas


title: SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [RNA-seq]

summary:
To investigate Chaetocin impact on Diffuse intrinsic pontine gliomas treatment
We then performed gene expression profiling analysis using data obtained from RNA-seq of Chaetocin treatment and SUV39H1 knockdown in SU-DIPG36 cells

overall_design: Comparative gene expression profiling analysis of RNA-seq data for  control SU-DIPG36 cells, Chaetocin treatment  cells and  SUV39H1 knockdown cells


title: The landscape of enhancer transcription in prostate cancer

first: Zezhong

last: Xiong

institute: Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology


title: Paraventricular nucleus CRH neurons regulate acute lung injury via sympathetic nerve–neutrophil axis [neutrophil]

status: Public on Feb 07 2025

city: Changsha

first: Dai

last: Ruping

state: Hunan

address: Ren-Min Central Road

institute: The Second Xiangya Hospital of Central South University

summary: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe conditions with high morbidity and mortality, and effective treatments are limited. Neuroimmune interactions play a critical role in lung homeostasis, but it remains unclear if specific brain regions regulate lung inflammation. Here, we unveil the critical role of neuroimmune signaling in ALI, focusing on the regulatory function of corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) of the hypothalamus. Using viral tracing, chemogenetic modulation, and pharmacological interventions in mouse models of ALI induced by intranasal lipopolysaccharide and cecal ligation and puncture (CLP), we found that lung injury activated CRHPVN neurons that projected to the lung. Activation of these neurons protected mice from ALI and death, reducing neutrophil infiltration and effector functions in the lung. In contrast, inhibiting CRHPVN neurons exacerbated ALI. Notably, the beneficial impact of CRHPVN neuron activation is compromised by the pulmonary chemical sympathectomy or inhibition of the β2-adrenergic receptor. These protective effects were dependent on sympathetic nerves, with norepinephrine released locally to modulate neutrophil functions via β2-AR–β-arrestin2 signaling, inhibiting the NF-κB pathway. Our findings reveal a brain-lung axis that regulates immune responses in ALI, suggesting novel therapeutic targets for ALI and ARDS.

overall_design: CRH-IRES-Cre mice were injected with AAV2/9-Ef1α-DIO-mCherry (control group) or AAV2/9-Ef1α-DIO-hM3Dq-mCherry (experimental group) into the paraventricular nucleus (PVN). After viral expression, CNO was intraperitoneally injected, and 1 hour later, LPS (20 mg/kg) was administered intranasally to induce acute lung injury (ALI). Neutrophils in the lung were isolated using magnetic beads after 24 h of modeling for neutrophil bulk RNA-seq.

first: Ruping

last: Dai

first: Hui

last: Li


city: Lausanne

first: Gaby

last: El Alam

state: Vaud

address: Station 15

department: SV LISP

institute: École polytechnique fédérale de Lausanne

summary:
Acute kidney injury (AKI) with maladaptive repair induces transition to chronic kidney disease (CKD) through inflammation, oxidative stress, and inappropriate homeostatic responses, including senescence and apoptosis. Here, we demonstrate that administration of cyclo Histidine-Proline (Cyclo His-Pro, CHP) protects against kidney injury and progression to CKD. Exogenous CHP pre-treatment preserved kidney function and produced significant reduction in tubular injury, apoptosis, and inflammatory cell infiltration in an ischemia-reperfusion injury (IRI) model. Compared with 5/6 nephrectomy (Nx) control rats, kidney function was protected and fibrosis was attenuated in CHP-treated 5/6 Nx rats. CHP also improved kidney injury in a unilateral ureteral obstruction (UUO) model with both prophylactic and therapeutic treatment regimens. To translate our observations to the human setting, we evaluated the relationship between endogenous CHP levels and CKD progression. As kidney function deteriorated, plasma CHP concentration increased, whereas tissue expression of Nrf2 displayed a negative relationship with CKD progression, suggesting that plasma CHP levels increase as a compensatory process to enhance the Nrf2 pathway activity. The data presented here support the efficacy of exogenous CHP treatment in preventing AKI-to-CKD transition potentially through Nrf2 pathway activation.
Results: Cyclo (His-Pro) is an effective treatment for the AKI-to-CKD Transition

overall_design:
Design: The purpose of this study was to investigate the effect of CHP on renal protection and provide support for its potential therapeutic use in human kidney disease. IRI mice model that represented the AKI was used to examine the protective effect of CHP. Then, we tested microarray analysis with IRI mice kidneys, to identify the renal protection mechanisms of CHP at the transcriptomic level. We tested hypoxia-reoxygenation model and H2O2 oxidative stress induction model with primary cultured hTECs to evaluate the anti-oxidant, anti-inflammatory, and renoprotective effect of CHP in AKI in vitro model. Assessment was performed in UUO in vivo model to determine the inhibitory effect of CHP on AKI to CKD transition. Potential prophylactic and therapeutic effects of CHP was analyzed in UUO mice model. To evaluate the renoprotective effect of CHP on CKD, We used 5/6 Nx rat model.
RNA sequencing using 5/6 nephrectomized rat kidneys was performed to study the effects at the molecular level. For in vitro experiments, primary cultured hTECs and podocytes were induced by various types of stress such as TGFβ or H2O2 to assess the anti-apoptotic and anti-fibrotic effect of CHP treatment. The associations between endogenous CHP level and CKD progression in humans were assessed by measuring CHP concentration with plasma and urine samples derived from CKD patients. The study was not blinded.

first: Jong

last: Moon

first: Yong

middle: C

last: Kim

first: Hoe-Yune

last: Jung

first: Jae

last: Lee

first: Won

last: Ju

first: Hyun

first: Adrienne

last: Mottis

last: Alam

first: Hajeong

first: Dong

first: Johan

last: Auwerx

first: Yon

first: Seung

middle: H

last: Yang


title: Osteocytes regulate transcortical blood vessel network by transferring mitochondria to endothelial cells in cortical bone

first: Junjie

last: Gao

address: 600 Yishan Road

institute: Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine

summary: In this study, mitochondria were proved to be capable of delivering mitochondria to endothelial cells of transcortical blood vessel and promotes its angiogenesis. By utilizing RNA seq, we investigated the effect of osteocytes-derived mitochondria on endothelial cells.

overall_design: bEnd.3 cells were co-cultured with or without mitochondria isolated from MLO-Y4 cells in vitro. After 24 hours, bEnd.3 cells were collected for further RNA-Seq analysis.

first: Peng


title: CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (CRTC2-RIPseq)

first: meixi

last: wang

overall_design: To investigate the cooperative function CRTC2-YTHDF2 co-condensates in N6-methyladenosine modificated mRNA fate transition, RIP-seq for CRTC2 was applied to identify targets gene in HCCLM3 cells.


title: PTP inhibition improves the macrophage anti-tumor immune response and the efficacy of chemo- and radiotherapy [GeoMX profiling]

city: Birmingham

first: Nestor

last: Prieto-Dominguez

state: AL

department: Microbiology

institute: The University of Alabama at Birmingham (UAB)

summary: Traditional anti-cancer therapies induce tumor cell death and subsequent release of Damage Associated Molecular Patterns (DAMPs) that activate the innate inflammatory response. Paradoxically, after treatment macrophages often adopt a pro-wound healing phenotype that contributes to cancer progression. We found that tumor cells upregulate the expression of Pros1 in areas proximal to cell damage. Tumor-secreted Pros1 binds to the macrophage Mer receptor, effectively limiting responsiveness to DAMPs by preventing Toll Like Receptor (TLR) signal transduction. Pharmacologically inhibiting PTP1b signaling downstream of Mer rescues the pro-inflammatory response even in the presence of Pros1. Combining PTP inhibition with traditional therapeutics, like chemo- or radiotherapy, rescues the innate immune response to DAMPs, increases immune infiltration, and causes 40-90% reductions in tumor growth in multiple treatment refractory preclinical models. Our findings suggest a novel use for PTP1b inhibitors as a tumor agnostic means of improving the efficacy of some of the most widely used anti-cancer therapeutic agents.

overall_design: GeoMX profiling of PanCK+ and CD45+ areas of B16F10 syngeneic murine tumors treated with PBS (iq, qd), cisplatin (5mg/kg, ip, once daily for three days), BVT948 (10mg/kg, ip, qd) or their combination collected 6 days after the start of the treatment. Regions of interest were picked based on gH2Ax expression, Pros1 expression, and Mer-Stat1 colocalization positive and negative areas. PanCK+ (melanoma fraction) and CD45+ (immune fraction) sections were manually determined using GeoMx DSP instruments and fluorescent antibodies against these proteins.

first: Jared

middle: P

last: Taylor

first: Eric

last: Ubil

first: Camilla

last: Bell


title: Comprehensive Analysis of DNA Methylation Patterns in Recurrent Miscarriage: Imprinted Genes and Their Regulation Across Sperm and Fetal-Maternal Tissues

city: Zhanjiang

first: Tianzhong

last: Ma

address: 57 People Avenue South

department: Reproductive Medicine Center

institute: Affiliated Hospital of Guangdong Medical University

type: Methylation profiling by genome tiling array

summary: Genome-wide DNA methylation profiling was performed on sperm (n=3) and chorionic villi (n=3) from RM patients and control couples undergoing artificial abortion using the Illumina HumanMethylation 450 BeadChip platform. Genes related with differentially methylated probes (DMPs) in functionally critical genomic regions, including enhancers, promoters, and DNase hypersensitive sites (DHS) were identified, and submitted to Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses.

overall_design: Bisulphite converted DNA from the 12 samples were treated to the Illumina Infinium® HumanMethylation450 BeadChip


title: An Environmental Toxin-Based Approach to Revealing c-MYC as the Key Regulator of Embryo Compaction

city: Beijing

first: Jianying

last: Hu

state: 北京

address: No. 5 Yiheyuan Road， Haidian District

institute: Peking University

summary: Compaction is a pivotal developmental event during the preimplantation development of mammalian embryos. However, the mechanisms underlying the initiation of compaction, especially transcription factors, remain poorly understood. Here, we established an environmental chemical-based focused screening strategy to identify new regulators of compaction. Using a morula-like aggregate model derived from mouse extended pluripotent stem cells, we screened a targeted chemical library of environmental toxins associated with female reproductive toxicity and identified perfluorooctanoic acid (PFOA) as a compound that disrupts compaction. Importantly, PFOA inhibits compaction in both morula-like aggregate model and mouse early embryos by downregulating the activity of transcription factor c-MYC. Mechanistically, c-MYC regulates the miR-200/ZEB/E-cadherin axis which drives cell-cell adhesion during the compaction process of early embryos. Our study uncovers c-MYC as a key transcription factor in regulating compaction of mouse embryos, providing novel insight into the mechanism of compaction regulation.

overall_design: RNA-seq profiling of morula-like aggregate model derived from mouse expanded pluripotent stem cells after treatment with PFOA or vehicle control.

first: Yanan

last: Liu

first: Xianlei

last: Jiang

first: Chenke

last: Xu

first: Chenhao

last: Zhang

first: Jun


title: Buprenorphine induces human fetal membrane sterile inflammation

city: New Haven

first: Hanah

last: Georges

state: Connecticut

address: 333 Cedar St

institute: Yale University

summary: Opioid-use disorder (OUD) during pregnancy has increased in the United States to critical levels and is a leading cause of maternal morbidity and mortality. Untreated OUD is associated with pregnancy complications in particular, preterm birth. Medications for OUD, such as buprenorphine, are recommended with the added benefit that treatment during pregnancy increases treatment post-partum. However, the rate of preterm birth in individuals using illicit opioids or being treated with opioid agonist therapeutics is double that of the general population. Since inflammation in the placenta and fetal membranes (FM) is a common underlying cause of preterm birth, we sought to determine if the opioid, buprenorphine, induces sterile inflammation in human FMs and to examine the mechanisms involved. Using an established in vitro human FM explant system, we report that buprenorphine significantly increased FM secretion of the inflammatory cytokine IL-6; the neutrophilic chemokine IL-8; and the inflammasome-mediated cytokine IL-1b, mirroring the inflammatory profile commonly seen at the maternal-fetal interface in preterm birth. Other factors that were elevated in FMs exposed to buprenorphine included the mediators of membrane weakening, prostaglandin E2 (PGE2), and the matrix metalloproteinases, MMP1 and MMP9. Furthermore, this sterile inflammatory and weakening FM response induced by buprenorphine was mediated in part by innate immune Toll-like receptor 4 (TLR4), the NLRP3 inflammasome, the m-opioid receptor, and downstream NFkB and ERK/JNK/MAPK signaling. This may provide the mechanistic link between opioid use in pregnancy and the elevated risk for preterm birth. Since there are adverse consequences of not treating OUD, our findings may help identify ways to mitigate the impact opioids have on pregnancy outcomes while allowing the continuation of maintenance therapy.

overall_design: Fetal membranes treated with buprenorphine (Bup) or without (Media; no treatment control), RNA extracted and sent for RNA seq

first: Tatyana

last: Lynn

first: Megan

last: Kelleher

first: Elle

last: McCauley

first: Ryan

middle: W

last: Logan

first: Kimberly

middle: A

last: Yonkers

first: Vikki

last: Abrahams


title: Cross-Tissue Comparison of Epigenetic Aging Clocks in Humans

city: University Park

first: Idan

last: Shalev

state: PA

address: 219 Biobehavioral Health Building

institute: The Pennsylvania State University

summary: Epigenetic clocks are a common group of tools used to measure biological aging – the progressive deterioration of cells, tissues and organs. Epigenetic clocks have been trained almost exclusively using blood-based tissues but there is growing interest in estimating epigenetic age using less-invasive oral-based tissues (i.e., buccal or saliva) in both research and commercial settings. However, differentiated cell types across body tissues exhibit unique DNA methylation landscapes and age-related alterations to the DNA methylome. Applying epigenetic clocks derived from blood-based tissues to estimate epigenetic age of oral-based tissues may introduce biases. We tested the within-person comparability of common epigenetic clocks across four tissue types: buccal epithelial, saliva, dry blood spots, and peripheral blood mononuclear cells. We tested 163 distinct tissue samples from 47 individuals aged 19-70 years. Overall, there were significant within-person differences in epigenetic clock estimates from oral-based versus blood-based tissues, with average differences of almost 30 years observed in some age clocks. In addition, most epigenetic clock estimates of blood-based tissues exhibited low correlation with estimates from oral-based tissues despite controlling for cellular proportions and other technical factors. Notably, the Skin and Blood clock exhibited the lowest age acceleration values of any clock across all tissue types, indicating its unique ability to accurately estimate chronological age in both oral- and blood-based tissues. Our findings indicate that application of blood-derived epigenetic clocks in oral-based tissues may not yield comparable estimates of epigenetic age, highlighting the need for careful consideration of tissue type when estimating epigenetic age. NOTE: The full study included children and adult samples, however, the current data only includes the adult samples (sample sizes and age range have been adjusted to reflect the adult data only).

overall_design: Trained phlebotomists performed antecubital venipuncture to collect 20 mL of whole blood in EDTA tubes. PBMCs were isolated from these whole blood samples through density-gradient centrifugation using Ficoll. Approximately 200 µL of whole blood were applied to a Whatman 903 protein saver card for the dried blood spot (DBS) samples. Participants were also asked to provide 4 mL of saliva across two Oragene tubes (OGR-500, DNA Genotek), which upon completion was mixed with Oragene stabilizing buffer and sealed. Eight buccal samples were collected using Isohelix SK1 swabs to firmly scrape the inside of the cheek per manufacturer’s directions. Collection order for all tissue types was uniform across participants. Participants were asked to refrain from eating or drinking anything other than water for one hour before collection. After collection, tissue samples were stored as follows: PBMCs were stored at -80°C in a solution buffer composed of phosphate buffered saline pH 7.2+EDTA (2mMol) + bovine serum albumin (0.5%) prior to DNA extraction. DBS were stored in sealed Ziploc bags with desiccant packets at room temperature. Buccal swabs were placed in sealed Ziploc bags and stored at -80°C. Saliva samples were aliquoted into 4 cryovials and stored at -80°C.


title: Differential and synergistic transcriptional effects of early amyloid-β and tau pathologies in the hippocampus of APP, Tau, and APP/Tau female mice

city: Bellaterra, Barcelona

first: Arnaldo

last: Parra-Damas

address: Campus UAB, Edifici M, M2-003

department: Biochemistry and molecular biology

country: Spain

institute: Universitat Autònoma de Barcelona

summary: Alzheimer’s disease (AD) is characterized by memory loss associated with accumulation of amyloid-β (Aβ) and tau in the brain, but how memory-processing neural circuits are differentially affected by each pathology remains unclear. Here, we investigated the transcriptional vulnerability to single and concomitant Aβ and tau pathologies in 6-month-old transgenic mice expressing mutant human amyloid precursor protein (APP), Tau, or both (APP/Tau mice) in excitatory neurons. We identified differential and synergistic pathology-induced transcriptional responses in the hippocampus of AD transgenic mice. These findings support the idea that Aβ and tau pathologies exert synergistic effects to disrupt gene expression programs underlying vulnerability of memory neural circuits in AD.

overall_design: To study the effect of single and concomitant early amyloid-β (Aβ) and tau neuropathologies on memory-processing circuits, 6-month-old APP, Tau, and double transgenic APP/Tau female mice were trained in the Morris water maze (MWM), and the bulk hippocampal transcriptomes were analyzed.

first: Ángel

last: Deprada

first: Carlos

last: Saura


title: Transcriptional vulnerability to amyloid-β and tau pathologies differentially disrupts emotional and memory neural circuits

summary: Alzheimer’s disease (AD) is characterized by memory loss and neuropsychiatric symptoms associated with cerebral accumulation of amyloid-β (Aβ) and tau, but how memory and emotional neural circuits are disrupted by AD pathology remains unclear. Here, we investigated the transcriptional vulnerability of memory and emotional circuits to concomitant Aβ and tau pathologies in transgenic mice expressing mutant human amyloid precursor protein (APP) and Tau (APP/Tau mice) in excitatory neurons. At 9 months, we detected common and region-specific transcriptional responses in the hippocampus and basolateral amygdala (BLA) of APP/Tau mice, including astrocytic, microglia and 63 AD-associated genes. These findings suggest that Aβ and tau pathologies disrupt region-specific gene expression programs underlying vulnerability of memory and emotional circuits to AD neuropathology.

overall_design: To study the effect of concomitant amyloid-β (Aβ) and tau neuropathology on memory- and emotion-processing circuits, 9-month-old double transgenic APP/Tau mice were trained in a cued fear conditioning/extinction paradigm, and the bulk transcriptomes of the basolateral amygdala (BLA) and hippocampus were analyzed.

first: Maria Dolores

last: Capilla-López


title: HDAC10 and Its Implications in Sézary Syndrome Pathogenesis

city: Poznań

first: Katarzyna

last: Iżykowska

state: Great Poland

address: Strzeszyńska 32

country: Poland

institute: Institute of Human Genetics PAS

summary: Cutaneous T-cell lymphomas (CTCL) are a group of rare hematological malignancies characterized by infiltration of malignant T-cells into the skin. Two main types of CTCL constitute of Mycosis Fungoides (MF), a more indolent form of the disease, and Sézary Syndrome (SS), the aggressive and leukemic variant with blood involvement. Sézary syndrome presents a significant clinical challenge due to its very aggressive nature, poor prognosis, and treatment resistance, and to date, the disease is known to be uncurable. Histone deacetylase inhibitors have gained attention in CTCL treatment with promising results, but they expose limited specificity and strong side effects. Recent genomic studies underscore the role of epigenetic modifiers in CTCL pathogenesis, prompting an investigation into HDAC10, a member of Class IIb HDACs, in SS. HDAC10 was investigated in different cancers, revealing its involvement in the cell cycle regulation, apoptosis, and autophagy, but its role in CTCL is unknown.  In this study we aimed to determine the role of HDAC10 in Sezary Syndrome, focusing on its cellular localization, role in cell growth, and potential therapeutic target. We indicated that HDAC10 is overexpressed in SS patients and located mainly in the cytoplasm. Its overexpression leads to an inhibitory effect on apoptosis progression when exposed to the pro-apoptotic compound Camptothecin (CPT). Knockdown of HDAC10 resulted in reduced cell growth and induction of apoptosis and autophagy, highlighting its potential importance in CTCL pathogenesis. Whole transcriptome analysis indicated that HDAC10 is associated with crucial cancer-related pathways for example hematopoietic cell lineage, PI3K-Akt signaling pathway, pathways in cancer, Ras signaling pathway, MAPK signaling pathway or JAK-STAT signaling pathway, which are critical for the survival and proliferation of malignant T cells. Inhibition of HDAC10 with selective HDAC10i increased the sensitivity of Sézary cells to the pro-apoptotic compound camptothecin (CPT). Our findings demonstrate that HDAC10 plays a key role in the molecular background of Sézary syndrome, highlighting its importance in the cellular mechanisms of the disease

overall_design: To investigate the biological role of class II histone deacetylase HDAC10 in Sezary syndrome, HDAC10 overexpression and knockdown were performed in two model CTCL cell lines SeAx and Hut78, and changes in gene expression and signaling pathways were analyzed using RNAseq.

first: Monika

last: Pieniawska

first: Karolina

last: Rassek

first: Bogumiła

last: Skwara

first: Magdalena

last: Żurawek

first: Iwona

last: Ziółkowska-Suchanek

first: Lydia

last: Visser

first: Monique

last: Lodewijk

first: Małgorzata

last: Sokołowska-Wojdyło

first: Berenika

last: Olszewska

first: Roman

last: Nowicki

first: Tomasz

last: Stein

first: Aleksandra

last: Dańczak-Pazdrowska

first: Adriana

last: Polańska

first: Marta

last: Szymoniak-Lipska

first: Natalia

last: Rozwadowska


title: Multiomic analysis uncovers a continuous spectrum of differentiation and Wnt-MDK-driven immune evasion in hepatoblastoma

city: Münster

first: Kornelius

last: Kerl

address: Albert-Schweitzer-Campus 1

department: Department of Pediatric Hematology and Oncology

country: Germany

institute: University Children's Hospital Münster

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

overall_design: Refer to individual Series


title: RNAseq on striatal bulk tissue of Dclk3 KO mice

city: strasbourg

first: Charles

last: DECRAENE

address: 12 rue Goethe

department: UMR 7364 CNRS

institute: CNRS

summary: To characterize striatal transcriptome of Dclk3 KO mice

overall_design: Comparative gene expression profiling analysis of RNA-seq data for Dclk3 KO and WT adult mice (12 months)

first: Karine

last: Merienne

last: Decraene

first: Emmanuel

last: Brouillet