title: Differentially expressed miRNAs in granulosa cell of diminished ovarian reserve (DOR) patients

city: Beijing

first: XiaoKui

last: Yang

address: 251, Yaojiayuan Road, Chaoyang DIstrct

country: China

institute: Beijing Obstetrics and Gynecology Hospital, Capital Medical University

summary: To investigate the pathogenesis of diminished ovarian reserve, differentially expressed miRNAs in granulosa cells were constructed through miRCURYTM LNA expression Array.

platform_organism:
Homo sapiens
Mus musculus
Rattus norvegicus
Human alphaherpesvirus 1
Human alphaherpesvirus 2
Human betaherpesvirus 5
Murid betaherpesvirus 1
human gammaherpesvirus 4
JC polyomavirus
Human immunodeficiency virus 1
Murid gammaherpesvirus 4
Human gammaherpesvirus 8
Merkel cell polyomavirus
Mus musculus cytomegalovirus 2
Betapolyomavirus hominis
Betapolyomavirus macacae

overall_design: In the study presented here, granulosa cells were collected from 3 DOR patients and 3 normal cycling women, respectively.

first: Sha

last: Peng

first: Xiaokui


title: MiR-106a increases granulosa cell viability and is down-regulated in women with diminished ovarian reserve

status: Public on Mar 14 2018

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

overall_design: Refer to individual Series


title: Widespread domain-like perturbations of DNA methylation in whole blood of Down syndrome neonates

status: Public on Mar 19 2018

city: Amsterdam

first: Peter

last: Henneman

state: Noord Holland

address: Meibergdreef 9

department: Clinical Genetics

country: Netherlands

institute: Academic Medical Center Amsterdam

type: Methylation profiling by genome tiling array

summary: Epigenetic (N=15) were based on the Illumina Infinium HumanMethylation450 BeadChip. We searched for differentially methylated probes (DMPs) and regions (DMRs).

overall_design: Bisulphite converted DNA obtained from whole blood were analysed using the the Infinium HumanMethylation450 BeadChip array

first: P

first: Arjan

last: Bouman

first: Adri

last: Mul

first: Lia

last: Knegt

first: Anne-Marie

last: van der Kevie-Kersemeakers

first: Nitash

last: Zwaveling-Soonawala

first: Hanne

middle: E

last: Meijers-Heijboer

first: A

middle: P

last: van Trotsenburg

first: M

middle: M

last: Mannens


title: Expression data from WT and RGS5 KO mice treated with DOCA/salt

city: Mannheim

first: Carsten

last: Sticht

address: Theodor-Kutzer-Ufer

department: ZMF

country: Germany

institute: University Heidelberg

summary: The activation of vascular smooth muscle cells (VSMCs) during hypertension-induced arterial remodeling processes relies on a change of the gene expression program, i.e., up-regulation of genes to induce migration, proliferation and matrix degradation/synthesis. At the same time, genes controlling the quiescent, contractile VSMC phenotype are down-regulated. We used microarrays to detail the global program of gene expression underlying hypertension-induced vascular remodeling in the presence and absence of regulator of G-protein signaling 5 (RGS5) and identified distinct classes of down-regulated genes during vascular remodeling when RGS5 was not present.

overall_design: WT and RGS5 KO mice (littermates) were treated with deoxycorticosterone acetate (DOCA; 50 mg/kg, 21-day-release pellets) and 1% NaCl in the drinking water for 10 days or left untreated. Afterwards, 2 femoral arteries per animal were isolated and RNA was extracted and hybridized on Affymetrix microarrays.

first: Caroline

last: Arnold

first: Thomas

last: Korff


title: Gene expression in the liver of mice infected with Fst288-AAV-TBG

city: boston

first: rongya

last: tao

state: MA

address: 300 Longwood Ave

country: USA

institute: boston children's hospital

summary:
We compared RNA expression profiles of wild type of mice maintained on high fat diet or Irs1/2:foxo1-LTKO mice infected with Fst288 AAV-TBG virus
Fst288-AAV-TBG infection modestly up- or down-regulated the expression of many genes, including several related to hepatic glucose metabolism (Pck1, G6pc and Gck) (Fig. S8a); qPCR confirmed that Fst288AAV•TBG affected the expression of these and other genes during both fasting (Pck1, G6pc and Gck) and feeding (Foxo1, Igfbp1, Pck1, and Ppargc1a)

overall_design: All mice were fasted and Liver were collected.

first: Morris

middle: F

last: White

first: Rongya

last: Tao


title: Differentially expressed miRNAs in serum of diminished ovarian reserve (DOR) patients

first: XiaoKui

last: Yang

summary: To investigate the pathogenesis of diminished ovarian reserve, differentially expressed miRNAs in serum were constructed through miRCURYTM LNA expression Array.

overall_design: In the study presented here, serum were collected from 3 DOR patients and 3 normal cycling women, respectively.

first: Sha

first: Xiaokui


title: Gene-expression analysis of human embryonic stem cell (HESC-)- derived rosette-forming neural progenitor cells (NPCs) in the presence of lysophosphatidic acid (LPA)

city: Vienna

first: Jan-Philip

last: Medelnik

state: Vienna

address: Campus-Vienna-Biocenter 1

country: Austria

institute: Research Institute of Molecular Pathology (IMP)

summary: As part of our study on the effect of LPA on HESC-derived NPCs, we have employed whole genome microarray analysis to identify genes which were up- and downregulated in the presence of LPA compared to non-LPA-treated control-NPCs and which might be involved in the expansion of the apical domain of NPCs and large rosette formation that we observe after LPA-treatment.

overall_design: Gene-expression of NPCs at rosette passaging number 2 (RP2) that were cultured in plastic 24-well plates and exposed for 2 h, 10 h and 24 h to 0.5 ml N2B27 + FGF2/EGF medium which was initially supplemented with 15 µM was performed. Experiments were performed in triplicates.


title: Gene expression in epigonadal white adipose tissue of LDKO and LTKO mice

summary:
We compared RNA expression profiles of eWAT obtained from Cntr- and LDKO-mice, and Cntr3- and LTKO-mice.
Compared against the controls, the expression of 82 genes decreased, and 83 genes increased more than 2-fold in eWAT of LDKO-mice, most of which returned to normal expression in eWAT of LTKO-mice

overall_design: Four month old LDKO and LTKO mice were fasted and epigonadal white adipose tissue were collected.


title: Characterizing the genetic background of nodal marginal zone lymphoma

status: Public on Mar 12 2018

city: Basel

first: Darius

last: Juskevicius

address: Schoenbeinstr. 40

department: Molecuar Pathology

country: Switzerland

institute: Institute of Pathology

type: Genome variation profiling by genome tiling array

summary: Nodal marginal zone lymphoma (NMZL) is a rare small B cell lymphoma lacking disease-defining phenotype and precise diagnostic markers. To better understand the mutational landscape of NMZL, particularly in comparison to other small nodal B cell lymphomas, we performed whole exome sequencing, targeted high throughput sequencing and array comparative genomic hybridization on a retrospective series. Our study identified for the first time recurrent, diagnostically useful and potentially therapeutically relevant BRAF mutations in NMZL. Sets of somatic mutations that could help to discriminate NMZL from other closely related small B cell lymphomas were uncovered and tested on unclassifiable small B cell lymphoma cases, in which clinical, morphological and phenotypical features were equivocal. Application of targeted gene panel sequencing gave at many occasions valuable clues for more specific classification.

overall_design: The dataset contains Agilent SurePrint 180k aCGH data for 22 nodal marginal zone lymphomas

first: Pillonel

middle: V

first: Charlotte

middle: K

last: Ng

first: Andrea

last: Bodmer

first: Andreas

last: Zettl

first: David

last: Jucker

first: Stefan

last: Dirnhofer

first: Alexandar

last: Tzankov


title: The expression profiles of circRNAs in hippocampus from mice with prenatal glyphosate exposure

status: Public on Mar 13 2018

city: HangZhou City

first: Hua

last: Ji

state: Zhejiang

address: No.481 Bingwen road

department: Department of Basic Medicine

institute: Hangzhou medical college

summary:
In this study, the circRNAs expression pattern in hippocampus of postnatal day (PND) 28 mice offsprings which were exposured by glyphosate-based herbicide (GBH) during pregnancy and lactation was investigated.
CircRNA microarray had detected 330 upregulated and 333 downregulated miRNAs in the PND28 mice offsprings' hippocampus

overall_design: In this study, the isolated total RNA taken from two pooled samples of two groups, was used to acquire expression profiles, and the result shows 663 differentially-expressed circRNAs, some of them are known to be involved in brain development or the pathogenesis of neurodevelopmental disorders, indicate that dysregulated expression of circRNAs may be involved in the mechanism of glyphosate-induced neurotoxicity.

first: Ni

last: Yu

first: Xinli

last: Fan


title: Nanostring of sorted lung conventional dendritic cells (cDCs) from cell-specific MyD88 KO at 6h after in vivo sensitization with OVA/standard flagellin

status: Public on Mar 10 2018

city: RTP

first: Seddon

last: Thomas

state: North Carolina

address: 111 T. W. Alexander Dr.,

institute: NIEHS

summary: Allergic asthma is a chronic disease of the airways characterized by eosinophilic and neutrophilic inflammation. MYD88, the adaptor molecule for TLR and IL-1 family member signaling, is required for allergic sensitization through the airway in animal models of allergic asthma. We generated conditionally mutant mice separately lacking Myd88 in airway epithelial cells (ECs) or dendritic cells (DCs) to define the contribution of Myd88 expression in each of these cell types. To examine crosstalk from ECs to conventional (c)DCs in vivo, we examined immune-specific transcriptional profiles from lung cDCs sorted following 6h in vivo lung allergic sensitization through the airways from WT MyD88 fx/fx, SPC cre+ MyD88 fx/fx (EC-MYD88 KO), CD11c cre+ MyD88 fx/fx (DC-MYD88 KO), and full MyD88 KO mice.  We observed immune-specific transcriptional changes in cDCs that were cell-intrinsic as well as resulting from in vivo crosstalk from ECs. We also observed transcriptional (linked data set) and epigenetic changes in chromatin conformation in cDCs by ATAC-seq (linked data set) as well as changes in immune-specific whole lung RNA, sorted EC RNA, and sorted alveolar macrophage (AM) RNA by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

overall_design: Lung cDCs from all genotypes were flow cytometry sorted following 6h of in vivo allergic sensitization with 100 micrograms ovalbumin (OVA)/ 1250 ng standard flagellin (stFLA). Samples from all 4 genotypes (WT MyD88 fx, SPC cre+ MyD88 fx, CD11c cre+ MyD88 fx, MyD88 KO) x 1 timepoints (6 h OVA/stFLA) = 4 conditions. 4 conditions x 3-4 replicates per genotype-timepoint = 14 total samples. WT MyD88 fx/fx mice are a positive control for all genes induced following allergen sensitization, while MyD88 KO is a negative control for genes that are not induced in the full body MyD88 KO mouse. SPC cre+ MyD88 fx/fx mice test for genes that require EC-dependent MYD88 signaling, whereas CD11c cre+ MyD88 fx/fx mice test for genes that require CD11c-expressing cell-dependent MYD88 expression. Gene expression analysis was conducted using using nCounter Mouse Immunology Codeset (Nanostring, Seattle, WA) on 3-4 biological replicates for each genotype and timepoint.

middle: Y

first: Donald

middle: N

last: Cook


title: RNA-seq from animals treated, and non treated,  with cisplatin

city: Hospitalet de Llobregat

first: Julián

last: Cerón

state: Barcelona

address: Gran via 199, Hospital Duran i Reynals, planta 3

department: Cancer and Human Molecular Genetics

country: Spain

institute: IDIBELL

type: Expression profiling by high throughput sequencing

summary: Transcriptome analysis of a population of control animals vs cisplatin-treated, in duplicate

overall_design: A mixed population of worms representing all stages and growing under control conditions was exposed to 60 µg/ml of cisplatin for 24 hours at 20ºC. Treated and control samples weer collected in biological replicates.

middle: C

last: Madrigal

first: Francisco

middle: J

last: García-Rodríguez


title: Nanostring of whole lung RNA from cell-specific MyD88 KO at 0h, 2h and 6h after in vivo sensitization with OVA/standard flagellin

summary: Allergic asthma is a chronic disease of the airways characterized by eosinophilic and neutrophilic inflammation. MYD88, the adaptor molecule for TLR and IL-1 family member signaling, is required for allergic sensitization through the airway in animal models of allergic asthma. We generated conditionally mutant mice separately lacking Myd88 in airway epithelial cells (ECs) or dendritic cells (DCs) and alveolar macrophages (AMs) to define the contribution of Myd88 expression in each of these cell types. To examine crosstalk between ECs and CD11c-expressing cells in vivo, we examined transcriptional profiles from whole lung RNA at baseline, or following 2h or 6h in vivo lung allergic sensitization through the airways from WT MyD88 fx/fx, SPC cre+ MyD88 fx/fx (EC-MYD88 KO), CD11c cre+ MyD88 fx/fx (DC-MYD88 KO), and full MyD88 KO mice.  We observed immune-specific transcriptional changes in whole lung RNA that were altered based on EC- or CD11c-specific deletion of MYD88. We also observed transcriptional (linked data set) and epigenetic changes in chromatin conformation in cDCs by ATAC-seq (linked data set) as well as changes in immune-specific sorted EC RNA, sorted AM RNA, and sorted cDC RNA by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

overall_design: Whole lung RNA was isolated from all genotypes were at baseline or following 2h or 6h of in vivo allergic sensitization with 100 micrograms ovalbumin (OVA)/ 1250 ng standard flagellin (stFLA). Samples from all 4 genotypes (WT MyD88 fx, SPC cre+ MyD88 fx, CD11c cre+ MyD88 fx, MyD88 KO) x 3 timepoints (baseline or 2h or 6h OVA/stFLA) = 12 conditions. 12 conditions x 3 replicates per genotype-timepoint = 36 total samples. Analysis of baseline (0h) timepoint is a control for induced gene changes.  WT MyD88 fx/fx mice are a positive control for all genes induced following allergen sensitization, while MyD88 KO is a negative control for genes that are not induced in the full body MyD88 KO mouse. SPC cre+ MyD88 fx/fx mice test for genes that require EC-dependent MYD88 signaling, whereas CD11c cre+ MyD88 fx/fx mice test for genes that require CD11c-expressing cell-dependent MYD88 expression. Gene expression analysis was conducted using nCounter Mouse Immunology Codeset (Nanostring, Seattle, WA) on 3 biological replicates for each genotype and timepoint.


title: Gene expression in kidney of interleukin-18 knockout mice at 6 and 12 weeks of age

status: Public on Mar 09 2018

city: Suita

first: Daisuke

last: Okuzaki

state: Osaka

address: Yamadaoka 3-1

department: Immunology Frontier Research Center

country: Japan

institute: Osaka univ.

summary: Interleukin-18 knockout mice had metabolic syndromes after 24 weeks of age. We examined gene expression profiles in mice kidney using genome-wide microarray technology, and compared gene expression profiles between wild-type and interleukin-18 knockout mice. To verify responsible molecules involved in metabolic syndromes such as obesity, we compared the gene expression levels at 6 and 12 weeks of age, and picked up them whose expression was more than 2-fold increase or less than 1/2-fold decrease.

overall_design: The mouse whole kidneys derived from wild type and interleukin-18 knockout mice at 6 and 12 weeks of age were examined. Each strain was run in triplicate.

first: Kyosuke

last: Yamanishi


title: Transcriptional profiling of Schneider cells to identify dGcn2 target genes after 12 hours expression

status: Public on Mar 07 2018

city: CAMBRIDGE

last: Marciniak

state: Cambridgeshire

address: Cambridge Biomedical Campus, Hills Road

department: CIMR (Cambridge Institute for Medical Research )

country: United Kingdom

institute: University of Cambridge; School of Clinical Medicine

summary: Transcriptional profiling of Schneider 2 cells comparing control  cells with stable inducible dGcn2-V5 expressing cells after 12h of induction with 0.7mM copper sulphate.

overall_design: Two-condition experiment: control  S2 cells vs. stable inducible S2 dGcn2-V5.pMT-Puro cells after 12h induction with 0.7 mM copper sulphate. Experiment was performed in three independent biological replicates.

first: Elke

last: Malzer

first: Caia

middle: S

last: Dominicus

first: Joseph

last: Chambers

first: Souradip

last: Mookerjee


title: Nanostring of sorted airway epithelial cells (AECs) from cell-specific MyD88 KO at 2h after in vivo sensitization with OVA/standard flagellin

summary: Allergic asthma is a chronic disease of the airways characterized by eosinophilic and neutrophilic inflammation. MYD88, the adaptor molecule for TLR and IL-1 family member signaling, is required for allergic sensitization through the airway in animal models of allergic asthma. We generated conditionally mutant mice separately lacking Myd88 in airway epithelial cells (ECs) or dendritic cells (DCs) and alveolar macrophages (AMs) to define the contribution of Myd88 expression in each of these cell types. To examine crosstalk from CD11c-expressing cells to ECs in vivo, we examined immune-specific transcriptional profiles from lung ECs sorted following 2h in vivo lung allergic sensitization through the airways from WT MyD88 fx/fx, SPC cre+ MyD88 fx/fx (EC-MYD88 KO), CD11c cre+ MyD88 fx/fx (DC-MYD88 KO), and full MyD88 KO mice.  We observed immune-specific transcriptional changes in ECs that were cell-intrinsic but none resulting from in vivo crosstalk from CD11c-expressing cells. We also observed transcriptional (linked data set) and epigenetic changes in chromatin conformation in cDCs by ATAC-seq (linked data set) as well as changes in immune-specific whole lung RNA, sorted AM RNA, and sorted cDC RNA by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

overall_design: Airway epithelial cells (ECs) from all genotypes were flow cytometry sorted following 2h of in vivo allergic sensitization with 100 micrograms ovalbumin (OVA)/ 1250 ng standard flagellin (stFLA). Samples from all 4 genotypes (WT MyD88 fx, SPC cre+ MyD88 fx, CD11c cre+ MyD88 fx, MyD88 KO) x 1 timepoint (2 h OVA/stFLA) = 4 conditions. 4 conditions x 2-3 replicates per genotype-timepoint = 1 total samples. WT MyD88 fx/fx mice are a positive control for all genes induced following allergen sensitization, while MyD88 KO is a negative control for genes that are not induced in the full body MyD88 KO mouse. SPC cre+ MyD88 fx/fx mice test for genes that require EC-dependent MYD88 signaling, whereas CD11c cre+ MyD88 fx/fx mice test for genes that require CD11c-expressing cell-dependent MYD88 expression. Gene expression analysis was conducted using nCounter Mouse Immunology Codeset (Nanostring, Seattle, WA) on 2-3 biological replicates for each genotype.


title: Transcriptional profiling of Schneider cells to identify crc target genes after 6 hours expression

summary: Transcriptional profiling of Schneider 2 cells comparing control stable inducible HA-expressing cells with stable inducible HA-crc expressing cells after 6h of induction with 0.7mM copper sulphate.

overall_design: Two-condition experiment, control cells stable inducible S2 HA.pMT-Puro cells vs. stable inducible S2 HA-crc.pMT-Puro cells after 6h induction with 0.7 mM copper sulphate. experiment was performed in three independent biological replicates.


title: Array of sorted lung conventional dendritic cells (cDCs) from cell-specific MyD88 KO at 0h and 6h in vivo sensitization with OVA/standard flagellin

summary: Allergic asthma is a chronic disease of the airways characterized by eosinophilic and neutrophilic inflammation. MYD88, the adaptor molecule for TLR and IL-1 family member signaling, is required for allergic sensitization through the airway in animal models of allergic asthma. We generated conditionally mutant mice separately lacking Myd88 in airway epithelial cells (ECs) or dendritic cells (DCs) to define the contribution of Myd88 expression in each of these cell types. To examine crosstalk from ECs to conventional (c)DCs in vivo, we examined transcriptional profiles from lung cDCs sorted at baseline or following 6h in vivo lung allergic sensitization through the airways from WT MyD88 fx/fx, SPC cre+ MyD88 fx/fx (EC-MYD88 KO), CD11c cre+ MyD88 fx/fx (DC-MYD88 KO), and full MyD88 KO mice.  We observed specific transcriptional changes in cDCs that were cell-intrinsic as well as resulting from in vivo crosstalk from ECs. We also observed epigenetic changes in chromatin conformation in cDCs by ATAC-seq (linked data set) as well as changes in immune-specific whole lung RNA, sorted EC RNA, sorted alveolar macrophage RNA, and sorted cDC by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

overall_design: Lung cDCs from all genotypes were flow cytometry sorted at baseline or following 6h of in vivo allergic sensitization with 100 micrograms ovalbumin (OVA)/ 1250 ng standard flagellin (stFLA). Samples from all 4 genotypes (WT MyD88 fx, SPC cre+ MyD88 fx, CD11c cre+ MyD88 fx, MyD88 KO) x 2 timepoints (0h baseline, 6 h OVA/stFLA) = 8 conditions. 8 conditions x 2 replicates per genotype-timepoint = 16 total samples. Analysis of baseline (0h) timepoint is a control for induced gene changes.  WT MyD88 fx/fx mice are a positive control for all genes induced following allergen sensitization, while MyD88 KO is a negative control for genes that are not induced in the full body MyD88 KO mouse. SPC cre+ MyD88 fx/fx mice test for genes that require EC-dependent MYD88 signaling, whereas CD11c cre+ MyD88 fx/fx mice test for genes that require CD11c-expressing cell-dependent MYD88 expression. Gene expression analysis was conducted using Affymetrix Mouse Transcriptome 1.0 arrays (Affymetrix, Santa Clara, CA) on 2 biological replicates for each genotype and timepoint.


title: Transcriptional profiling of Schneider cells to identify crc target genes after 3 hours expression

summary: Transcriptional profiling of Schneider 2 cells comparing control stable inducible HA-expressing cells with stable inducible HA-crc expressing cells after 3h of induction with 0.7mM copper sulphate.


title: Nanostring of sorted lung alveolar macrophages (AM) from cell-specific MyD88 KO at 6h after in vivo sensitization with OVA/standard flagellin

summary: Allergic asthma is a chronic disease of the airways characterized by eosinophilic and neutrophilic inflammation. MYD88, the adaptor molecule for TLR and IL-1 family member signaling, is required for allergic sensitization through the airway in animal models of allergic asthma. We generated conditionally mutant mice separately lacking Myd88 in airway epithelial cells (ECs) or dendritic cells (DCs) and alveolar macrophages (AMs) to define the contribution of Myd88 expression in each of these cell types. To examine crosstalk from ECs to AMs in vivo, we examined transcriptional profiles from lung AMs sorted following 6h in vivo lung allergic sensitization through the airways from WT MyD88 fx/fx, SPC cre+ MyD88 fx/fx (EC-MYD88 KO), CD11c cre+ MyD88 fx/fx (DC-MYD88 KO), and full MyD88 KO mice.  We observed immune-specific transcriptional changes in AMs that were cell-intrinsic as well as resulting from in vivo crosstalk from ECs. We also observed transcriptional (linked data set) and epigenetic changes in chromatin conformation in cDCs by ATAC-seq (linked data set) as well as changes in immune-specific whole lung RNA, sorted EC RNA, and sorted cDC RNA by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

overall_design: Alveolar macrophages from all genotypes were flow cytometry sorted following 6h of in vivo allergic sensitization with 100 micrograms ovalbumin (OVA)/ 1250 ng standard flagellin (stFLA). Samples from all 4 genotypes (WT MyD88 fx, SPC cre+ MyD88 fx, CD11c cre+ MyD88 fx, MyD88 KO) x 1 timepoint (6 h OVA/stFLA) = 4 conditions. 4 conditions x 2 replicates per genotype-timepoint = 8 total samples. WT MyD88 fx/fx mice are a positive control for all genes induced following allergen sensitization, while MyD88 KO is a negative control for genes that are not induced in the full body MyD88 KO mouse. SPC cre+ MyD88 fx/fx mice test for genes that require EC-dependent MYD88 signaling, whereas CD11c cre+ MyD88 fx/fx mice test for genes that require CD11c-expressing cell-dependent MYD88 expression. Gene expression analysis was conducted using nCounter Mouse Immunology Codeset (Nanostring, Seattle, WA) on 2 biological replicates for each genotype.


title: Gene expression signatures before or after transient middle cerebral artery oclussion (tMCAO) in ZEB1 transgenic and wild type mice

city: Tianjin

first: Junwei

last: Hao

address: 154 Anshan Road, Heping District

institute: Tianjin Medical University General Hospital

summary: To further development of the role of ZEB1 in microglia, we have employed whole mRNA microarray expression profiling as a discovery platform to identify genes.  Mouse microglia from wild type(wt), ZEB1-overexpression(ZEB1-tg) and ZEB1 knock down(ZEB1-kd) mice were isolated before and after tMCAO. The result showed after tMCAO, the wild type, ZEB1-overexpression and ZEB1 knock down microglia displayed a different gene profile, this suggested microglia ZEB1 might play an important role after ischemic stroke.

overall_design: We first assessed the gene expressions in wild type, ZEB1-overexpression and ZEB1 knock down microglia before tMCAO. Then we measured the gene expressions in wild type, ZEB1-overexpression and ZEB1 knock down microglia after tMCAO.


title: Hereditary Hearing Loss SNP-Microarray Pilot Study

status: Public on Mar 06 2018

city: Wuerzburg

first: Barbara

last: Vona

state: Bavaria

address: Biozentrum, Am Hubland

department: Institute of Human Genetics

institute: University of Wuerzburg

summary:
Objectives: Despite recent advancements in diagnostic tools, the genomic landscape of hereditary hearing loss remains largely uncharacterized. One strategy to understand genome-wide aberrations includes the analysis of copy number variation that can be mapped using SNP-microarray technology. A growing collection of literature has begun to uncover the importance of copy number variation in hereditary hearing loss. This pilot study underpins a larger effort that involves the stage-wise analysis of hearing loss patients, many of whom have advanced to high-throughput sequencing analysis.
Data description: Our data originate from Infinium HumanOmni1-Quad v1.0 SNP-microarrays (Illumina) that provide useful markers for genome-wide association studies and copy number variation analysis. This dataset comprises a cohort of 108 individuals (99 with hearing loss, 9 normal hearing family members) for the purpose of understanding the genetic contribution of copy number variations to hereditary hearing loss.

overall_design: To investigate the genome-wide controbution of copy number variation, we hybridized 108 individuals (99 with hearing loss, 9 unaffected family members) on the InfiniumHuman Omni1-Quad v1.0 SNP-microarrays (Illumina).

first: Thomas

last: Haaf


title: Transcriptional profiling of Schneider cells to identify dGcn2 target genes after 6 hours expression

first: Stefan

summary: Transcriptional profiling of Schneider 2 cells comparing control  cells with stable inducible dGcn2-V5 expressing cells after 6h of induction with 0.7mM copper sulphate.

overall_design: Two-condition experiment: control  S2 cells vs. stable inducible S2 dGcn2-V5.pMT-Puro cells after 6h induction with 0.7 mM copper sulphate. Experiment was performed in three independent biological replicates.


title: BLIMP-1 is insufficient to induce antibody secretion in the absence of IRF4

status: Public on Mar 05 2018

city: Turku

first: Paulina

last: Budzynska

address: Kiinamyllynkatu 13

country: Finland

institute: University of Turku

summary: Differentiation of B cells into antibody secreting cells (ASCs), plasmablasts and plasma cells, is regulated by a network of transcription factors. Within this network factors including PAX5 and BCL6 prevent ASC differentiation and maintain the B cell phenotype whereas BLIMP-1 and high IRF4 expression promote plasmacytic differentiation. BLIMP-1 is thought to induce immunoglobulin secretion. While IRF4 is needed for the survival of ASCs, its role in the regulation of antibody secretion has been controversial. BCL6-deficient DT40 B cell line has upregulated BLIMP-1 expression and secrete antibodies. In order to study the role of IRF4 in regulation of antibody secretion we have created a double knockout (DKO) DT40 B cell line deficient in both IRF4 and BCL6. This DKO cell line did not upregulate PRDM1 (the gene encoding for BLIMP-1) expression or secrete IgM. Even enforced BLIMP-1 expression in DKO cells or IRF4-deficient cells could not induce IgM secretion while it did in WT cells. However, enforced IRF4 expression in DKO cells induced strong IgM secretion. Our findings support a model where IRF4 expression in addition to BLIMP-1 expression is required to induce antibody secretion.

overall_design: Gene expression profiles of BCL6 knockout (BCL6KO) and IRF4-BCL6 doubleknockout (DKO)  chicken DT40 B cells were generated by Agilent Chicken Gene Expression Microarray V2.

first: Minna

last: Kyläniemi


title: Chip-SIP analysis of Pacifica pier surface waters incubated with organic and inorganic nitrogen and carbon substrates

status: Public on Mar 03 2018

city: Livermore

first: Xavier

last: Mayali

state: CA

address: 7000 East Ave

department: Chemical Science

institute: Lawrence Livermore National Laboratory

summary:
October 2010 surface seawater collected from Pacifica pier was incubated with 14 different substrates for 12 hours.
Community RNA was extracted and hybridized to a Roche Nimblegen microarray and analyzed by NanoSIMS to obtain isotope ratio data for all probe spots.

overall_design: Three Chips for fluorescence, and 14 Chips for different substrates from samples incubated for 12 hours.


title: Androgen Deprivation Therapy Potentiates the Efficacy of Vascular Targeted Photodynamic Therapy of Prostate Cancer Xenografts

city: New York

first: Nicholas

middle: D.

last: Socci

state: NY

address: 1275 York Ave

department: bioinformatics core

institute: Memorial Sloan Kettering Cancer Center

summary: WST11 vascular targeted photodynamic therapy (VTP) is a local ablation approach relying upon rapid, free radical-mediated destruction of tumor vasculature. A phase III trial showed that VTP significantly reduced disease progression when compared to active surveillance in patients with low-risk prostate cancer (PCa). The aim of this study was to identify a druggable pathway that could be combined with VTP to improve its efficacy and applicability to higher risk PCa tumors.

overall_design:
LNCaP-AR cells were grafted into intact mice to establish tumors. The mice were then treated with WST11 at 9 mg/kg, and tumors were focally treated with VTP using 100 mW laser fluence.
Tumors were collected at 3, 6, or 24 hr, 1 week and 8.5 weeks post VTP. Mice with control tumors received WST11, but were not exposed to the laser and were matched to the 1 and 8.5 week treatment groups.
RNA was isolated from 36 total tumors for microarray hybridization, with 4-8 replicates per group. 32 samples were used for analysis (n=4 from 24 hr VTP removed during quality control).

first: Kwanghee

last: Kim

first: Philip

middle: A

last: Watson

first: Jonathan

last: Coleman


title: Daytime variation of perioperative myocardial injury in cardiac surgery and its prevention by Rev-Erbα antagonism: a single-centre propensity-matched cohort study and a randomised study

city: Lille

first: Lefebvre

last: Philippe

state: Nord

address: Blvd Pr. J.Leclerc

country: France

institute: Inserm

summary: Background On-pump cardiac surgery provokes a predictable perioperative myocardial ischaemia–reperfusion injury which is associated with poor clinical outcomes. We determined the occurrence of time-of-the-day variation in perioperative myocardial injury in patients undergoing aortic valve replacement and its molecular mechanisms. Methods We studied the incidence of major adverse cardiac events in a prospective observational single-centre cohort study of patients with severe aortic stenosis and preserved left ventricular ejection fraction (>50%) who were referred to our cardiovascular surgery department at Lille University Hospital (Lille, France) for aortic valve replacement and underwent surgery in the morning or afternoon. Patients were matched into pairs by propensity score. We also did a randomised study, in which we evaluated perioperative myocardial injury and myocardial samples of patients randomly assigned (1:1) via permuted block randomisation (block size of eight) to undergo isolated aortic valve replacement surgery either in the morning or afternoon. We also evaluated human and rodent myocardium in ex-vivo hypoxia–reoxygenation models and did a transcriptomic analysis in myocardial samples from the randomised patients to identify the signalling pathway(s) involved. The primary objective of the study was to assess whether myocardial tolerance of ischaemia–reperfusion differed depending on the timing of aortic valve replacement surgery (morning vs afternoon), as measured by the occurrence of major adverse cardiovascular events (cardiovascular death, myocardial infarction, and admission to hospital for acute heart failure). The randomised study is registered with ClinicalTrials.gov, number NCT02812901. Findings In the cohort study (n=596 patients in matched pairs who underwent either morning surgery [n=298] or afternoon surgery [n=298]), during the 500 days following aortic valve replacement, the incidence of major adverse cardiac events was lower in the afternoon surgery group than in the morning group: hazard ratio 0·50 (95% CI 0·32–0·77; p=0·0021). In the randomised study, 88 patients were randomly assigned to undergo surgery in the morning (n=44) or afternoon (n=44); perioperative myocardial injury assessed with the geometric mean of perioperative cardiac troponin T release was significantly lower in the afternoon group than in the morning group (estimated ratio of geometric means for afternoon to morning of 0·79 [95% CI 0·68–0·93; p=0·0045]). Ex-vivo analysis of human myocardium revealed an intrinsic morning–afternoon variation in hypoxia–reoxygenation tolerance, concomitant with transcriptional alterations in circadian gene expression with the nuclear receptor Rev-Erbα being highest in the morning. In a mouse Langendorff model of hypoxia–reoxygenation myocardial injury, Rev-Erbα gene deletion or antagonist treatment reduced injury at the time of sleep-to-wake transition, through an increase in the expression of the ischaemia–reperfusion injury modulator CDKN1a/p21. Interpretation Perioperative myocardial injury is transcriptionally orchestrated by the circadian clock in patients undergoing aortic valve replacement, and Rev-Erbα antagonism seems to be a pharmacological strategy for cardioprotection. Afternoon surgery might provide perioperative myocardial protection and lead to improved patient outcomes compared with morning surgery.

overall_design: Patients in both the cohort study and randomised study underwent aortic valve replacement either in the morning or in the afternoon by one of the four senior surgeons who operated twice every working day: the same surgical team did both morning and afternoon surgery on the same day. Anaesthaesia, cardiopulmonary bypass, cardioplegia, and surgical procedures were done according to standard guidelines. Anaesthesia was induced with intravenous sufentanil (1·0–1·5 μg/kg) and propofol (0·5–1·5 mg/kg), and maintained with endtidal sevoflurane (1·7% of the expired fraction). Surgery was done using normothermic cardiopulmonary bypass and repeated antegrade cold crystalloid-blood cardioplegia. Right atrial biopsy was obtained during pulmonary bypass preparation. Total RNA was extracted from human tissues and analysed on Agilent SurePrintG3 HumanGeneExpression 8x60Kv2 (Agilent, Santa Clara, CA, USA)

first: P

last: Lefebvre

first: D

last: Montaigne


title: Interfering with interferons: cholesterol modification by Helicobacter pylori prevents IFN receptor assembly

status: Public on Mar 02 2018

city: Berlin

first: Hans-Joachim

last: Mollenkopf

address: Charitéplatz 1

institute: Max-Planck-Institute for Infection Biology

summary: Interferons (IFNs) are thought to primarily protect against intracellular pathogens. Here we show that Helicobacter pylori, a chronic colonizer of gastric mucosal surfaces, effectively blocks both type I and type II IFN signalling via cholesterol-α-glucosyltransferase (CaGT). Thus, CaGT, causing depletion of cholesterol from host cells, prevents infected epithelial cells from executing crucial effector functions, including the production of human b-defensin 3 (hBD3). Cholesterol depletion by CaGT prevents the assembly of interferon receptors resulting in a failure of JAK/STAT1 activation and subsequent expression of downstream transcriptional regulators (IRF-1 and 7), T-cell chemo-attractants (CXCL9 and 10) and antimicrobial peptides. Moreover, infection of human primary gastric epithelial cells by H. pylori also prevents residual type I IFN autocrine signalling and thereby further dampens the response to type II IFNs. Our results uncover a cooperative role for type I and type II IFNs in the defense against extracellular bacteria and explain the mechanism by which cholesterol modification by H. pylori usurps epithelial cell effector function, normally triggered by T-cell-derived inflammatory signals. Accordingly, CaGT acts as a central pathogenesis determinant and immune modulator of H. pylori contributing to this pathogen's exceptional ability of life-long persistence.

overall_design: Microarray experiments were performed as dual-color hybridizations on Agilent-026652 human whole genome catalog 44K arrays. To compensate for dye-specific effects, a dye-reversal independent color-swap with two biological replicates was applied. Microarray image data were analyzed and processed with the Image Analysis/Feature Extraction software G2567AA v. A.11.5.1.1 (Agilent Technologies) using default settings and the GE2_1105_Oct12 extraction protocol.

first: Pau

last: Morey

first: Lennart

last: Pfannkuch

last: Meyer

first: Hans


title: Transgenerational DNA methylation changes in Daphnia magna exposed to chronic gamma radiation

status: Public on Mar 01 2018

city: Saint Paul lez Durance

first: olivier

last: ARMANT

address: Cadarache BP3

department: SERIS

institute: IRSN

type: Methylation profiling by high throughput sequencing

summary: DNA methylation epigenetic changes were analysed in Daphnia magna exposed for 25-day to chronic gamma irradiation compared to unexposed controls.  Generation F0 were exposed to 6.5 μGy/h or 41.3 mG/h and let recoverd until the F3 generation without exposures to ionizing radiations. DNA-methylation  patterns were analysed by WGBS on the whole organismes at the generation F0, F2 and F3 in order to detect possible transmission of DNA methylation changes to the progeny.

overall_design: Biological samples (whole adults) were analysed by WGBS

first: Olivier

last: Armant

first: Marie

last: Trijau

first: Frederique

last: Alonzo


title: Transcriptome related to pubertal development in Brahman heifers

city: Brisbane

first: Marina

last: Fortes

state: Queensland

address: SCMB, room 454 bld 76

department: School of Chemistry and Molecular Biosciences

country: Australia

institute: The University of Queensland

summary: here we report the data from six pre-puberty and six post-puberty Brahman heifers, tissue samples collected in liquid nitrogen for RNA sequencing (mRNA libraries)

overall_design: RNA sequencing for six tissues in Brahman

first: Stephen

last: Moore


title: Characterization of Transcriptomes of Apical OHCs and Basal OHCs in Cochlea

city: Xi'an

first: Jianhua

last: Qiu

state: Shaanxi

address: 127 West Changle Rd

department: Otolaryngology Head & Neck Surgery

institute: Xijing Hospital, Fourth Military Medical University

summary: We analyzed the transcriptomes of 30 isolated apical OHCs and basal OHCs from rat cochlea, and the results showed that more than 50 genes were differentially expressed and 20 genes were uniquely expressed among these populations. We analyzed these genes with a focus on their functions related to cellular structure and transmembrane channels and their vulnerability to and involvement in hereditary deafness caused by OHC defects. Our results could serve as a guideline for exploring the molecular mechanisms underlying the biological properties of OHCs.

overall_design: 2 sub-populations of cochlear outer hair cells with different gene expression related to thair differences in structure, function and vulnerability

first: Yang

first: Meihao

last: Qi


title: Tumor evolution in the context of castration resistance in prostate cancer

first: Joël

middle: Roman

last: Federer-Gsponer

address: Tangentenweg 34

department: Department of Pathology

institute: University Hospital Basel

summary: Clinical resection specimens of prostate tissue (radical prostatectomy and TUR-P) over the course of hormone deprivation therapy were flow sorted according to their DNA content (Ploidy) and subjected to aCGH analysis to identify possiple chromosomal abberations which could confer castration resistance.

overall_design: 7 Patients where multiple timepoints were avaiable were first flow sorted according to DNA content and then hypridized on Agilent aCGH arrays.

middle: R

first: Cristina

last: Quintavalle

first: David

last: Müller

first: Tanja

last: Dietsche

first: Valeria

last: Perrina

first: Thomas

last: Lorber

first: Darius

last: Juskevicius

first: Elisabeth

last: Lenkiewicz

first: Tobias

last: Zellweger

last: Gasser

first: Michael

middle: T

last: Barrett

first: Cyrill

last: Rentsch

first: Lukas

last: Bubendorf

first: Christian

last: Ruiz


title: Transcription Factor-Mediated Control of Anthocyanin Biosynthesis in Vegetative Tissues of Tomato

status: Public on Jan 30 2018

city: Wageningen

first: Jules

last: Beekwilder

address: Droevendaalsesteeg 1

institute: Wageningen Plant Research

summary: DEX inducible expression system for Rosea1 and Delila transcription factors was introduced in tomato. Seedlings and callus tissues were induced by DEX. RNA of induced and uniniduced roots and calli was isolated after 3 and 24h.

first: Rumyana

last: Karlova


title: Identification of Transcripts Associated with Renal Damage Due to Ureteral Obstruction as Candidate Urinary Biomarkers

status: Public on Feb 22 2018

city: Stanford

first: Bo

last: Wu

state: Ca

address: 300 Pasteur Dr. Grant/S259

department: Urology

institute: Stanford University

summary:
Renal obstruction is a common cause of renal failure in adults and children and is suspected when hydronephrosis is detected on imaging.  Since not all cases of hydronephrosis are associated with renal damage, biomarkers are needed to guide intervention to relieve obstruction.  We performed gene expression profiling on the kidneys from adult mice over a detailed time course after obstruction and compared these data to a neonatal model of bilateral high grade obstruction induced by conditional deletion of the calcineurin ß1 (Cnb1) gene.  Using a model of short term (non-damaging) and long term (damaging) temporary obstruction, we identified which of the transcripts common to the adult and neonatal models were induced early and associated with renal damage.  Using QPCR, elevated levels of several candidate RNA biomarkers of renal damage were detected in urine from obstructed mice and children undergoing surgery for ureteropelvic junction obstruction (UPJO).
This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Mechanistic differences in neuropathic pain modalities revealed by correlating behavior with global expression profiling [microarray]

status: Public on Jan 19 2018

city: Los Angeles

first: Giovanni

last: Coppola

address: 1524 Gonda, 695 Charles Young Drive South

department: Psychiatry and Neurology

institute: UCLA

summary: Chronic neuropathic pain is a major morbidity of neural injury, yet its mechanisms are incompletely understood. Hypersensitivity to previously non-noxious stimuli (allodynia) is a common symptom. Here, we demonstrate that the onset of cold hypersensitivity precedes tactile allodynia and this temporal divergence was associated with major differences in global gene expression in dorsal root ganglia (DRG). Transcripts whose expression correlate with the onset of cold allodynia were nociceptor-related, whereas those correlating with tactile hypersensitivity were enriched for immune cell activity. Selective ablation of TrpV1 lineage nociceptors resulted in mice that did not acquire cold allodynia but developed normal tactile hypersensitivity. Whereas, depletion of macrophages or T cells reduced neuropathic tactile allodynia but not cold hypersensitivity. We conclude that neuropathic pain is contributed to by reactive processes of sensory neurons and immune cells, each leading to distinct forms of pain hypersensitivity, potentially allowing effective drug development targeted to each pain modality.

overall_design: High temporal analysis of global gene expression in the DRG following spared nerve injury (SNI) correlated with behavior taken at the same time points. Expression and behavioral sensitivity taken at least daily over the first 10 days post SNI.

first: E

last: Cobos

first: C

last: Nickerson

first: F

last: Gao

first: V

last: Chandran

first: I

last: Bravo-Caparrós

first: N

last: Andrews

first: A

last: Latremoliere

last: Joller

first: P

last: Riva

first: M

last: Painter

last: Ma

first: T

last: Omura

last: Chesler

first: D

middle: H

last: Geschwind

first: G

last: Rangachari

last: Woolf

last: Costigan


title: Perinatal paroxetine exposure in Selcetively-bred Low Responder rats

city: Blacksburg

first: Matthew

last: Glover

state: VA

address: 1981 Kraft Drive, Integrated Life Science

department: Neuroscience

institute: Virginia Tech

summary: Selective serotonin reuptake inhibitor (SSRI) antidepressants are the mainstay treatment for the 10-20% of pregnant and postpartum women who suffer major depression, but the effects of SSRIs on their children’s developing brain and later emotional health are poorly understood. SSRI use during pregnancy can elicit antidepressant withdrawal in newborns and increase toddlers’ anxiety and social avoidance. In rodents, perinatal SSRI exposure increases adult depression- and anxiety-like behavior, although certain individuals are more vulnerable to these effects than others. Our study establishes a rodent model of individual differences in susceptibility to perinatal SSRI exposure, utilizing selectively-bred Low Responder (LR) and High Responder (HR) rats that were previously bred for high versus low behavioral response to novelty. Pregnant HR/LR females were chronically treated with the SSRI paroxetine (10 mg/kg/day p.o.) to examine its effects on offspring’s emotional behavior and gene expression in the developing brain. Paroxetine treatment had minimal effect on HR/LR dams’ pregnancy outcomes or maternal behavior. We found that LR offspring, naturally prone to an inhibited/anxious temperament, were susceptible to behavioral abnormalities associated with perinatal SSRI exposure (which exacerbated their Forced Swim Test immobility), while high risk-taking HR offspring were resistant. Microarray studies revealed robust perinatal SSRI-induced gene expression changes in the developing LR hippocampus and amygdala (postnatal days 7-21), including transcripts involved in neurogenesis, synaptic vesicle components, and energy metabolism.  These results highlight the LR/HR model as a useful tool to explore the neurobiology of individual differences in susceptibility to perinatal SSRI exposure.

overall_design: 78 samples from 2 brain regions (hippocampus and amygdala) across four developmental timepoints (postnatal days (P)7, 14, 21, 75) following perinatal exposure paroxetine (or normal drinking water).

first: Sarah

last: Clinton


title: The gene microarray of digoxin on high-fat diet (HFD) induced changes in liver tissue

status: Public on Jan 08 2018

city: New Haven

first: Xinshou

last: Ouyang

state: CT

address: 1 Gilbert street

department: Internal Medicine

institute: Yale University

summary: The goals of this study are to measure the microarray profiling of digoxin treated group versus vehicle control group in a 12 weeks HFD induced gene changes in liver tissue. The 'WT_LIVER" samples are from mice fed normal chow and not treated with digoxin, and the "HFD-WT" samples are from mice fed a high-fat diet and not treated with digoxin.

overall_design: Liver tissue mRNA profiles of 12 weeks HFD in C57BL/6 mice were generated by Illumina mouse Ref-8 v2.0 expression BeadChips.

first: Wajahat

last: Metal


title: MDA-PCa-2b cells, Control vs. ARlnc1 knockdown, AR-regulated gene signature generated by DHT treatment

status: Public on Feb 16 2018

city: Ann Arbor

first: Marcin

middle: Piotr

last: Cieslik

state: Michigan

address: 500 S State St

department: Pathology

institute: University of Michigan

summary: (1) Transcription profiling of MDA-PCa-2b cells comparing ARlnc1 knockdown treated cells with control cells. Two methods were used to knockdown ARlnc1: siRNA or ASO. (2) Transcription profiling of MDA-PCa-2b cells comparing dihydrotestosterone (DHT) stimulated cells with vehicle treated cells. The goal is to determine AR-regulated gene expression signature in MDA-PCa-2b cells.

overall_design: (1) siRNA-mediated knockdown: cells transfected with 2 individual ARlnc1 siRNAs (si2 and si3), compared to non-targeting siRNA. (3 replicates each assay). (2) ASO-mediated knockdown: cells transfected with 2 individual ASOs targeting ARlnc1 (ASO2 and ASO6), compared to control ASO. (2 replicates each assay). (3) DHT-treated MDA-PCa-2b cells, compared to vehicle treated cells. (3 replicates)

first: Yajia

last: Zhang


title: Gene expression in peripheral blood Tcells from sows

status: Public on Jan 10 2018

city: Kyoto

first: Ryo

last: Inoue

address: 1-5, Hangi-cho, shimogamo

institute: Kyoto Prefectural University

summary: Whole blood was collected from sows and peripheral blood mononuclear cells (PBMC) were isolated. CD3+CD4+, CD3+CD8+ and CD3+CD4+CD8+ were separately sorted by a cell sorter. Transcriptional profile of each T cell subset was obtained.

overall_design: Comparison: CD3+CD4+ vs CD3+CD4+CD8+ and CD3+CD8+ and CD3+CD4+CD8+. Biological replicates; 3

first: R

last: Okutani


title: Stochastic gain of susceptibility suggests a novel mechanism of resistance to hybrid dysgenesis in Drosophila virilis

status: Public on Dec 20 2017

city: Moscow

first: Sergei

last: Funikov

state: Moscow

address: Vavilov str. 32

country: Russia

institute: Engelhardt Insitute of Molecular Biology

type: Non-coding RNA profiling by high throughput sequencing

summary: Syndromes of hybrid dysgenesis (HD) have been critical for our understanding of the transgenerational maintenance of genome stability by piRNA. HD in D. virilis represents a special case of HD since it includes simultaneous mobilization of a set of TEs that belong to different classes. The standard explanation for HD is that eggs of the responder strains lack an abundant pool of piRNAs corresponding to the asymmetric TE families transmitted solely by sperm. However, there are several strains of D. virilis that lack asymmetric TEs, but exhibit a “neutral” cytotype that confers resistance to HD. To characterize the mechanism of resistance to HD, we performed a comparative analysis of the landscape of ovarian small RNAs in strains that vary in their resistance to HD mediated sterility. We demonstrate that resistance to HD cannot be solely explained by a maternal piRNA pool that matches the assemblage of TEs that likely cause HD. In support of this, we have witnessed a cytotype shift from neutral (N) to susceptible (M) in a strain devoid of all major TEs implicated in HD. This shift occurred in the absence of significant change in TE copy number and expression of piRNAs homologous to asymmetric TEs. Instead, this shift is associated with a change in the chromatin profile of repeat sequences unlikely to be causative of paternal induction. Overall, our data suggest that resistance to TE-mediated sterility during HD may be achieved by mechanisms that are distinct from the canonical syndromes of HD.

overall_design: Deep-sequencing of ovarian small RNA from parental strains and the dysgenic and reciprocal crosses.


title: Gene expression analysis to find molecular mechanisms underlying the role of miR-342-5p in HER2 breast cancer

status: Public on Dec 21 2017

city: Oslo

first: Evita

last: Lindholm

address: Ullernchausseen 70

department: Genetics

country: Norway

institute: Oslo University Hospital, Radiumhospitalet

summary: The molecular mechanisms behind the miR-342-5p-induced HER2 pathway regulation are not known. Here, we aimed to further investigate the role of miR-342-5p in HER2 driven breast cancer cells. Transfected cells were incubated for 24 hours, and total RNA were run on mRNA arrays.

overall_design: Two HER2 amplified breast cancer cell lines were transiently transfected with miR-342-5p mimic or scrambled negative control miRNA. Transfections were done in three separate biological replicates.

first: Suvi

last: Leivonen

first: Eldrid

last: Due

first: Daniel

last: Nebdal

first: Anne-Lise

last: Børresen-Dale

first: Kristine

last: Sahlberg


title: 25D3 and 1,25D3 target gene profiles in LNCaP

status: Public on Dec 01 2017

city: Itabashi-ku

first: Takao

last: Susa

state: Tokyo

department: Department of Biochemistry

institute: Teikyo University School of Medicine

summary: Most prostate cancers depend on androgen and androgen receptor signaling for their proliferation and development, which underpins the efficacy of antiandrogens as powerful therapeutic agents for prostate cancers. On the other hand, interaction between AR and other nuclear hormone receptors (NRs) such as glucocorticoid receptor in the prostatic cancer or between AR and ER in breast cancers depicts the close association or “crosstalk” of AR with other NRs in terms of the new approach toward the management of hormone-resistant prostate/breast cancers. Along with this line, chemopreventive and antiproliferative action of 1,25(OH)2D3 (abbreviated as 1,25D3), an active metabolite of vitamin D3, during the management of prostate and/or breast cancers has been recently rigorously argued. We found that in its physiological concentration, 25(OH)D3 (abbreviated as 25D3), the precursor metabolite of 1,25D3 and widely-recognized as an inactive vitamin D because of its much weaker binding activity to vitamin D receptor (VDR) compared to 1,25D3, has a gene transcription profile similar to 1,25D3 in some prostate cancers. In this study, we investigated whole genome target gene profiles and intracellular behaviors of VDR after administration of 25D3 or 1,25D3 in prostate cancer LNCaP cells to elucidate the hormonal activity of 25D3. First, we confirmed that LNCaP cells possessed functional 25D3-VDR as well as 1,25D3-VDR signaling systems by qRT-PCR. By immunofluorescent examination of nuclear translocation, western blotting and most importantly, knockdown of CYP27B1 and/or VDR after the introduction of the respective siRNA into these cells, we found that, just like 1,25D3, 10-7 M of 25D3, which is within its uppermost physiological concentrations in the bloodstream, induced VDR nuclear import and robustly activated its target gene such as CYP24A1 in the virtual absence of CYP27B1 expression in LNCaP cells. These results indicate that the unconverted 25D3 alone behaved similarly to 1,25D3 in activating CYP24A1 mRNA expression. Our comprehensive microarray analyses verified the bioactivity of 25D3 and we found that 25D3 target gene profiles largely matched those of 1,25D3, while the presence a small subset of 25D3-, or 1,25D3-specific target genes were not excluded. The concentration of 1,25D3 in the culture media after 25D3 treatment with or without siRNA for CYP27B1 mRNA was below the lower limit of the sensitivity measured by ultrasensitive LC/MS/MS method. These results indicated that 25D3 shares bioactivity with 1,25D3 without conversion to the latter at least in some prostate cancer cells.

overall_design: Total RNA from the LNCaP cells transfected with control siRNA (siCT), siRNA for CYP27B1 (siCYP27B1) or siRNA for VDR (siVDR) followed by 10-7 M of 25D3 or 1,25D3 treatment for another 24 h was isolated using an RNeasy Mini Kit (Qiagen, Hilden, Germany) according to the manufacturer's instructions. RNA samples were quantified using an ND-1000 spectrophotometer (NanoDrop Technologies, Wilmington, DE), and their quality was confirmed using an Experion System (Bio-Rad Laboratories, Hercules, CA). cDNA microarray analysis was performed using an authorized custom analysis service provider.

first: Tomoki

last: Okazaki


title: Functions of peptides involved in cancer metastasis

status: Public on Dec 16 2017

city: Kurume

first: Michiyo

last: Tsuru

state: Fukuoka

address: 67 Asahimachi

department: Orthopardic Surgery

institute: Kurume Universuty

summary: We retrospectively investigated sera, obtained from 47 patients after the complete cure of liver cancer, using follow-up proteome analysis for 8 years, and found a protein, whose expression increased over time, peaked at the definitive diagnosis of bone metastases by bone scintigraphy, and tapered after the start of subsequent treatment.  Fractions obtained by the reverse-phase HPLC of this protein were digested with trypsin and examined by LC-MS/MS analysis.  The data were analyzed with a Mascot database search.  As a result, the mass of fragment 576-628 of the C-terminal region of alpha-fibrinogen precursor was 5,805, which corresponded to that of the target peak.  On the other hand, the mass of region 576-629 (with Val at the C-terminal) was 5,904, a mass value 99 higher than the target peak.  This corresponds to a peak detected in the serum sample at a mass value 100 higher than the target peak.  This peak with a mass value 100 higher was the same as the target peak in terms of chromatographic behavior, indicating that this peak had a protein sequence similar to that of the target peak.  The isoelectric point (pI) of the fragment of region 576-628 was 8.07.  This is consistent with the fact that the target peak indicates the behavior of a basic material in ion exchange.  Thus, we concluded that the target peak 5,813 was a fragment of C-terminal region 576-628 of the alpha-fibrinogen precursor.

overall_design: Vascular endothelial cells inherently control platelet functions and the coagulation and fibrinolytic system, and do not cause thrombus. A mixture of human lung cancer H460 cells and the target peptide was cultured, with normal human lung microvascular endothelial cells cultured on the 8.0-μm pore membrane of the upper layer and 3D Matrigel polymerized on the lower layer. Twenty-four hours later, the culture was examined by SEM electron microscopy to demonstrate that cancer cells grew on the 8.0-μm pore membrane and reached the normal human lung microvascular endothelial cells. Forty-eight hours later, neovessels were formed, around which platelet-containing thrombi were observed.

first: Michio

last: Sata

first: Maki

last: Tanaka

first: Kei

last: Matsuoka

first: Takaaki

last: Fukuda

first: Hideaki

last: Yamana

first: Yoshio

last: Kodera

first: Kensei

last: Nagata

last: Umeyama


title: Tumor Necrosis Factor Associated Factor 2 Mediates Cardiac Protection Through Non-canonical NF-κB Signaling

status: Public on Dec 15 2017

city: Indianapolis

first: Scot

last: Matkovich

state: IN

address: Lilly Corporate Center

institute: Eli Lilly and Company

summary:
To elucidate the mechanisms responsible for cytoprotective effects of tumor necrosis factor receptor activated factor 2 (TRAF2) in the heart, we employed genetic gain and loss of function studies ex vivo and in vivo in mice with cardiac restricted overexpression of TRAF2 (Myh6-TRAF2LC). Crossing Myh6-TRAF2LC mice with mice lacking canonical signaling (Myh6-TRAF2LC/Myh6-IκBαΔN) abrogated the cytoprotective effects of TRAF2 ex vivo. In contrast, inhibiting the JAK/STAT pathway did not abrogate the cytoprotective effects of TRAF2. Transcriptional profiling of wild-type, Myh6-TRAF2LC, Myh6-TRAF2LC/Myh6-IκBαΔN hearts suggested that the non-canonical NF-κB signaling pathway was upregulated in the Myh6-TRAF2LC hearts.
Western blotting and ELISA for the NF-κB family proteins p50, p65, p52 and RelB on nuclear and cytoplasmic extracts from naïve 12 week old wild-type, Myh6-TRAF2LC and Myh6-TRAF2LC/Myh6-IκBαΔN mouse hearts showed increased expression levels and increased DNA binding of p52 and RelB, which are NF-κB family members, whereas there was no increase in expression nor DNA binding of the p50 and p65 subunits. Crossing Myh6-TRAF2LCmice with RelB-/+mice (Myh6-TRAF2LC/RelB-/+) attenuated the cytoprotective effects of TRAF2 ex vivo and in vivo. Viewed together, these results suggest that cross-talk between the canonical and non-canonical NF-κB signaling pathways is required for mediating the cytoprotective effects of TRAF2.

overall_design: Hearts from WT, Myh6-TRAF2LC, Myh6-IκBαΔN and Myh6-TRAF2LC/Myh6-IκBαΔN (n = 4 per group) were used for transcriptional profiling.

first: Sarah

last: Evans

first: Douglas

middle: L

last: Mann


title: Analysis of influence of Excretory Secretory Products from wild and laboratory Fasciola hepatica isolates on LPS activated bovine macrophages

status: Public on Nov 01 2017

city: Warsaw

first: Piotr

last: Bąska

state: Mazowieckie

address: Ciszewskiego 8

department: Department of Preclinical Sciences

country: Poland

institute: Warsaw University of Life Sciences WULS – SGGW

summary: F. hepatica is a parasite causing losses of great importance in animal production. It is also considered a zoonosis of growing importance. During the infection the parasite releases a number of antigens (called Excretory Secretory Products - ESP) facilitating the parasites survival. A number of ESP components have immunomodulatory properties.  To determine if ES from various F. hepatica isolates have different immunomodulatory abilities LPS activated “BOMA” cells were stimulated with ES of laboratory Weybridge (FhWey-ES) and wild (FhWild-ES) Fasciola hepatica isolates.

overall_design: The experiment was performed in quadruplicate. Cells were seeded in 24 deep well plates. Four wells were stimulated and four were unstimulated and treated as controls. RNA was isolated from cells from each well followed by labelling with Cy3 (control cells) or Cy5 (stimulated cells). The material was hybrised to four bovine mRNA microarrays (Agilent).

first: Luke

last: Norbury

first: Kamil

last: Januszkiewicz


title: To compare the transcriptome of ompR null strains with wild-type strain of E. coli during acid or osmotic stress

status: Public on Nov 08 2017

city: singapore

first: smarajit

last: chakraborty

address: T-Lab, 5A Engineering Drive 1, NUS

country: Singapore

institute: Mechanobiology Institute

summary: In bacteria, one paradigm for signal transduction is the two-component regulatory system, consisting of a sensor kinase (usually a membrane protein) and a response regulator (usually a membrane protein) and a response regulator (usually a DNA binding protein). The EnvZ/OmpR two-component system in E. coli responds to osmotic stress and regulates expression of outer membrane proteins. Furthermore, bacteria were believed to regulate pH by acidifying after external acid stress, then immediately recovering. Using a pH-sensor in single living cells, we show that E. coli maintain an acidic cytoplasm. The osmotic stress transcription factor OmpR, was required. Thus, we set out to identify the OmpR targets under acid and osmotic stress.

sample_organism: Escherichia coli str. K-12 substr. MG1655

overall_design: To identify OmpR targets under acid and osmotic stress conditions, we performed a microarray and compared the transcriptome of ompR null strains with wild-type strains of E. coli during acid or osmotic stress. E. coli strain was grown in MgM media at pH 5.6, 7.2 and 7.2 with 15% (w/v) sucrose to O.D ~0.6.  The total RNA was isolated using an RNeasy mini kit (Qiagen) and proceeded for Microarray

first: Smarajit

last: Chakraborty

first: Linda

last: Kenney


title: Dectin1-Stimulated mTOR-C/EBPβ Signaling Induces IL-10-Producing Regulatory Tr2 Cells

status: Public on Oct 14 2017

city: Bethesda

first: Timothy

middle: G

last: Myers

state: MD

address: 50 South Drive, Room 5509

department: Research Technologies Branch

institute: National Institute of Allergy and Infectious Diseases

summary: In the present study we describe a new subset of murine T cells producing high levels of IL-10 that, in this case, are induced by C-type lectin receptor-stimulated (i.e., Dectin-1-stimulated) dendritic cells. This T cell produces IL-10 as a result of a transcriptional mechanism that is distinct from that inducing IL-10 in Th2 cells, Tr1 cells or other T cell subsets. In particular, the mechanism involves mTOR signaling and induction of the LIP isoform of C/EBPb, a factor that interacts with phospho-CREB and GATA3 to induce transactivation of the IL-10 gene. These T cells have strong regulatory properties in relation to fungal infection and hence have been termed Tr2 regulatory T cells to distinguish them from other regulatory T cell subsets.

overall_design: 4 types of T-cells measured in duplicate are compared.  1) T-BMDC sup-CD3 sup (T0), 2) T-BMDC sup-CD3+ZD(Tr2), 3) Th2, 4) Tr1.

first: Masaki

last: Tajima

first: Ivan

last: Fuss

first: Paul

last: Gardina

first: Atsushi

last: Kitani

first: Warren

last: Strober


title: Intestinal inflammatory regulation requires high-affinity TCR-ZAP70-mediated Runx3 activity in mice

status: Public on Nov 15 2017

city: Woolloongabba

first: Ahmed

middle: Murtaza

last: Mehdi

state: QLD

address: 37 Kent Street

department: Diamantina Institute

institute: The University of Queensland

summary: comparing gene expression of SKG and BALBc mice

overall_design: Total RNA was purified from terminal ileum of 8 naïve SKG and 3 naïve BALB/c mice using RNeasy kits (Qiagen). RNA from tissues selected for microarray (10 - 30mg, Bioanalyzer RNA Integrity Scores >6) was amplified using the TotalPrep RNA amplification kit (Ambion). Amplified RNA was hybrized to Illumina MouseRef-8 v2.0 Expression BeadChip arrays. Arrays were scanned on an Illumina iScan.


title: Genome-wide analysis of dorsal skin gene expression of control and K14-cre:Gab1fl mutant mice

status: Public on Dec 19 2017

city: Berlin

first: Ozlem

last: Akilli Ozturk

address: Robert Roesslestr. 10

department: Signal Transduction

institute: Max Delbruck Center

summary: Analysis of genes regulated by Gab1 mediated signaling in hair cycle initiation

overall_design: FACS sorted alpha6integrin+ cells from dorsal skin of control mice was compared to K14-cre; Gab1fl conditional mutant mice

first: Walter

last: Birchmeier


title: Transcriptomic analysis of lung tissue from cigarette smoke induced emphysema murine models and human COPD show shared and distinct pathways

status: Public on Sep 05 2017

city: Boston

first: Jeong

last: Yun

state: MA

address: 181 Longwood Ave

institute: BRIGHAM AND WOMEN'S HOSPITAL

summary: Although cigarette smoke (CS) is the primary risk factor for COPD, the underlying molecular mechanisms for the significant variability in developing COPD in response to CS are incompletely understood. We performed lung gene expression profiling of two different wild-type murine strains (C57BL/6J, NZW/LacJ) and two genetic models with mutations in COPD GWAS genes (HHIP, FAM13A) after 6 months of chronic CS exposure and compared the results to human COPD lung tissues. We identified gene response patterns that correlate with severity of emphysema in mouse and human lungs. Xenobiotic metabolism and Nrf2-mediated oxidative stress response were commonly regulated molecular response patterns across C57BL/6J, Hhip +/- and Fam13a -/- murine models upon chronic CS exposure and human COPD subjects.  The CS resistant Fam13a -/- mouse and NZW/LacJ strain revealed an opposite pattern of gene expression response, suggesting distinct molecular pathways for resistance against emphysema. There were few genes commonly modulated between mouse and humans. Our study suggests gene expression responses to CS may be largely species and model dependent, yet shared pathways could provide biologically significant insights underlying individual susceptibility to CS

overall_design: Total RNA was obtained from the lung tissue of C57BL/6J wild type, Hhip+/- , Fam13a -/- and NZW/LacJ exposed to cigarette smoke (CS) or filtered air (air) for 6 months and gene expression profiling was performed on murine lungs.

first: Jarrett

last: Morrow

first: Caroline

last: Owen

first: Weiliang

last: Qiu

first: Kimberly

last: Glass

first: Taotao

last: Lao

first: Zhiqiang

last: Jiang

first: Mark

last: Perrella

first: Edwin

last: Silverman

first: Xiaobo

last: Zhou

first: Craig

middle: P

last: Hersh


title: Mouse hepatoblastoma models with expression of mutant β-catenin and/or c-Myc for therapeutic target identification of childhood liver cancer

status: Public on Aug 23 2017

city: San Antonio

first: Yidong

last: Chen

state: Texas

address: 8403 Floyd Curl Drive, MSC 7784

department: Population Health Sciences

institute: UT Health Science Center at San Antonio

summary: Hepatoblastoma (HB), the most common type of pediatric liver cancer, is associated with aberrant wnt/β-catenin activation and Myc amplification/overexpression.  Mice expressing both alleles developed HBs and HCCs with incomplete penetrance by 5-6 weeks of age with fetal and mixed fetal/embryonal HBs, the most prevalent histologic HB subtypes seen in children being the predominant tumor types. To address the roles of mutant wnt/β-catenin activation and Myc over-expression in the pathogenesis of HB, c-Myc and mutant dominant-stable β-catenin were co-targeted to immature cells of the developing mouse liver.

overall_design: Whole genome gene expression profiling with Agilent 1 color protocol were performed to total of 11 samples (4 Wild types, 3 with mutant beta-catenin expression, and 4 with c-Myc expression) derived from tumor-bearing livers.

first: Sarah

last: Comerford

first: Elizabeth

last: Hinnant

first: Gail

middle: E

last: Tomlinson

first: Robert

last: Hammer


title: Transcription factor NFAT1 regulates systemic autoimmunity through modulation of dendritic cell property

status: Public on Jul 31 2017

city: Pohang

first: Sinhyeog

last: Im

state: Hyoja-dong Namgu

address: POSTECH, postech biotech center Rm 430, Hyoja-dong Namgu, pohang

country: South Korea

institute: POSTECH/IBS

summary: To characterize the roles of NFAT1 in the pathogenesis of autoimmune myasthenia gravis (MG) at a genome-wide scale, we performed gene expression microarray analysis for wild-type (WT) and NFAT1 KO bone marrow-derived dendritic cells (BMDCs) with or without 2h and 12h-stimulation with pam3CSK4.

overall_design: Total RNA was extracted from bone marrow derived dendritic cells of WT and NFAT1 KO with or without pam3CSK4 stimulation

first: Chang-Suk

last: Chae

first: Eun

last: Park

first: Choong-Gu

last: Lee

first: Gi-Cheon

last: Kim

first: Hagg-Lim

last: Cho

first: Chang-Duk

last: Jun

first: Sin-Hyeog


title: Genome-wide expression profiling analysis of a Hmgn2 and Hmgn1/2 double knock out mutant mouse model

status: Public on Oct 01 2017

city: Neuherberg

first: Martin

last: Irmler

state: Bayern

address: Ingolstaedter Landstrasse 1

department: Institute of Experimental Genetics

institute: Helmholtz Zentrum München GmbH

summary: DNase I hypersensitive sites (DHSs) are a hallmark of chromatin regions containing regulatory DNA such as enhancers and promoters; however, the factors affecting the establishment and maintenance of these sites are not fully understood. We now show that HMGN1 and HMGN2, nucleosome-binding proteins that are ubiquitously expressed in vertebrate cells, maintain the DHS landscape of mouse embryonic fibroblasts (MEFs) synergistically. Loss of one of these HMGN variants led to a compensatory increase of binding of remaining variant. Genome wide mapping of the DHSs in Hmgn1-/-, Hmgn2-/- and Hmgn1-/-n2-/- MEFs reveals that loss of both, but not a single HMGN variant, leads to significant remodeling of the DHS landscape, especially at enhancer regions marked by H3K4me1 and H3K27ac. Loss of HMGN variants affects the induced expression of stress responsive genes in MEFs, the transcription profiles of several mouse tissues, and leads to altered phenotypes that are not seen in mice lacking only one variant.  We conclude that the compensatory binding of HMGN variants to chromatin maintains the DHS landscape and the transcription fidelity necessary to retain wild type phenotypes. Our studies provide insights into mechanisms that maintain regulatory sites in chromatin and into functional compensation among nucleosome binding architectural proteins.

overall_design: total RNA of brain, liver, spleen and thymus from homozygote Hmgn2-/- and homozygote double knock out Hmgn1-/-n2-/- was compared to the corresponding wild type RNA from the C57BL/6 strain

first: Johannes

last: Beckers

first: Marion

last: Horsch


title: Infection with Streptococcus pneumoniae triggers progression of pulmonary fibrosis by pneumolysin

status: Public on Sep 01 2017

city: Jena

first: S.

last: Lambeck

address: Erlanger Allee 101

institute: JUH

summary:
A two-hit model of adenoviral vector delivery of active transforming growth factor-β (TGFb) 1 to induce fibrosis in mice in conjunction with treatment of the mice with purified pneumolysin from Streptococcus pneumoniae was applied to characterize the role of this virulence factor on fibrosis perpetuation in mice
The study was supported by a BMBF grant for the German Center for Lung Research, partner site BREATH (Biomedical Research in Endstage and Obstructive Lung Disease Hannover)

overall_design: Total RNA of murine lung type II alveolar epithelial cells of AdTGFb1 treated mice challenged with pneumolysin (PLY, n=4) and its non-cytotoxic derivative (PdB, n=3) were extracted and subjected to microarray analysis for contrasts of pneumolysin (PLY) versus control (PdB) treatment.

first: Sandro

last: Lindig

first: Ulrich

last: Maus


title: The role of ferritin heavy chain (Fth) in polymicrobial sepsis.

status: Public on Aug 15 2017

summary:
We systematically assessed the transcriptomic changes of livers of MxCreFthD/D vs. Fthlox/lox mice after induction of polymicrobial sepsis using Cecal Ligation and Puncture.
Data indicates a distinct set of genes differentially regulated between MxCreFthD/D and Fthlox/lox mice after sepsis induction reflecting altered iron and glucose metabolism.

overall_design: RNA from murine livers in MxCreFthD/D  and Fthlox/lox mice:  (n=4 for sepsis per genotype, n=4 for untreated controls per genotype) was extracted and subjected to microarray analysis for comparison of transcriptomic responses.

first: Sebastian

last: Weis

first: Miguel

last: Soares


title: Multi-tissue transcriptomics delineates the diversity of airway T cells functions in asthma

status: Public on Oct 02 2017

city: London

first: Akul

last: Singhania

address: 1 Midland Road

institute: The Francis Crick Institute

summary: Asthma arises from the complex interplay of inflammatory pathways in diverse cell types and tissues including epithelial and T cells.

overall_design: To undertake a comprehensive transcriptomic assessment of epithelium and airway T cells in asthma, and investigate the interactions between these tissues.

first: Christopher

last: Woelk

first: Timothy

last: Hinks


title: Retinal gene expression responses to aging are sexually divergent

status: Public on Jul 21 2017

city: Hershey

first: Penn State

last: COM

state: PA

address: 500 University Drive

department: Genome Sciences Facility

institute: Penn State College of Medicine

summary: Sex and age are critical factors in a variety of retinal diseases but have garnered little attention in preclinical models.  The current lack of knowledge impairs informed decision making on inclusion and design of studies incorporating both sexes and aging.  The goal of this study was to examine mouse retina normative gene expression in both sexes with advancing age.

overall_design: Retinal gene expression in female and male C57BL/6 mice at 3 months and 24 months of age were compared for sex differences and aging responses through whole transcriptome microarray analysis.

first: Colleen

last: Mangold

first: Benjamin

last: Wronowsk

first: Mei

last: Du

first: Dustin

last: Masser

first: Niran

last: Hadad

first: Georgina

middle: V

last: Bixler

first: Robert

middle: M

last: Brucklacher

first: Matthew

last: Ford

first: William

last: Sonntag

first: Willard

last: Freeman


title: Transcriptional profiling of GDF11 or TGFB1 stimulated NMuMG 3D spheroids

status: Public on Feb 13 2018

city: Charlottesville

first: Kevin

middle: A.

last: Janes

address: Box 800759 Health System

department: Department of Biomedical Engineering

institute: University of Virginia

summary:
The objective of this study was to identify transcriptional changes differentially regulated by GDF11 stimulation compared to TGFB1
Microarrays were used to capture the differential transcriptional response to acute GDF11 stimulation compared to acute TGFB1 stimulation

overall_design: NMuMG 3D spheroids were stimulated with 250 ng/mL GDF11, 50 ng/mL TGFB1, or serum-free media and evaluated at four hours after stimulation in biological quadruplicate.

first: Sameer

last: Bajikar


title: Revisiting the roadmap of medullary thymic epithelial cell differentiation

status: Public on Jul 28 2017

city: Heidelberg

first: Benedikt

last: Brors

address: Berliner str. 41

department: Applied Bioinformatics

institute: German Cancer Research Center

summary: The basic two-step terminal differentiation model of the medullary thymic epithelial cell (mTEC) lineage from immature MHCIIlo to mature MHCIIhi mTECs has recently been extended to include a third stage namely the post-Aire MHCIIlo subset as identified by lineage-tracing models. Yet, a suitable surface marker distinguishing the phenotypically overlapping pre- from the post-Aire immature MHCIIlo stage has been lacking. Here, we introduce the lectin Tetragonolobus purpureas agglutinin (TPA) as a novel cell surface marker that allows for such delineation. Based on our data, we derived the following sequence of mTEC differentiation: TPA- MHCIIlo → TPA- MHCIIhi → TPA+ MHCIIhi → TPA+ MHCIIlo. Surprisingly, in the steady-state postnatal thymus most immature TPA- pre-Aire rather than terminally differentiated post-Aire TPA+ MHCIIlo mTECs were marked for apoptosis at an exceptionally high rate of about 70 %. Hence, only the minor cycling fraction of the MHCIIlo subset (< 20 %) potentially qualified as mTEC precursors. FoxN1 expression inversely correlated with the fraction of slow cycling and apoptotic cells within the four TPA subsets. TPA further sub-divided human mTECs, though with different subset distribution. Our revised roadmap emphazises close parallels of terminal mTEC development with that of skin, undergoing an alternative route of cell death namely cornification rather than apoptosis. The high rate of apoptosis in immature pre-Aire mTECs points to a “quality control” step during early mTEC differentiation.

overall_design: Mouse medullary thymic epithelial cells were sorted with two markers: MHC-II high/low and TPA plus/minus. There are four groups: MHC-II low TPA minus, MHC-II high TPA minus, MHC-II high TPA plus, MHC-II low TPA plus. Each group has four replicates

first: Chloé

last: Michel

first: Rita

last: Küchler

first: Bruno

last: Kyewski

first: Sheena

last: Pinto


title: Transcriptomic analysis comparing mouse strains with extreme total lung capacities identifies novel candidate genes for pulmonary function

status: Public on Jul 26 2017

first: Johannes

last: Beckers

address: Ingolstaedter Landstr. 1

institute: Helmholtz Zentrum Muenchen

summary: Our data demonstrates enrichment of the GO term extracellular region among the decreased lung transcripts of JF1 throughout the process of lung development and maturation in consistent to the altered elastin to collagen ratio. Our microarray data showed increased ~4 fold increased elastin transcripts in JF1 lungs at P70. Specific CL‐saline/air ratio in JF1 mice compared to C3H (JF1-male: 2.68±01.10 versus C3H-male: 2.15±0.42, p<0.05; JF1-female: 3.22±0.88 versus C3H-female: 2.27±0.23, p<0.05) suggests that surface tension contributes more than the elastic recoiling properties of lung in determining the lung compliance as assessed by air filling. This observation is consistent with the smaller alveolar size of JF1 mice. The lower ratio (specific compliance) of CLAir/TLC and CLSaline/TLC in JF1 indicates that elastic recoil due to tissue properties is higher in JF1 compared to C3H. Therefore, the two phenomenon results in a less compliant lung due to higher surface tension in the alveoli and higher elastic recoil due to tissue properties in JF1 compared to C3H. Therefore, the lung architecture, lung function and molecular data of the two strains are in agreement with each other.

overall_design: We compare lung tissue of the two inbred strains C3H/HeJ and JF1/MsJ at three time points during lung development (embryonic day 18, postnatal days 28 and 70).

first: Leema

last: George

first: Ankita

last: Mitra

first: Tania

last: Thimraj

first: Martin

last: Irmler

first: Sangeetha

last: Vishweswaraiah

first: Lars

last: Lunding

first: Dorothea

last: Hühn

first: Alcia

last: Madurga-Hernandez

first: Heinz

last: Fehrenbach

first: Swapna

last: Upadhyay

first: Holger

last: Schulz

first: George

middle: D

last: Leikauf

first: Koustav

last: Ganguly


title: Transcriptomic analysis of conditional THAP1 knockout mice brains using microarray

status: Public on Jul 10 2017

first: Ravindran

last: Kumaran

address: 35 Lincoln Drive

institute: NIH

summary:
Loss of function mutations in the transcription factor THAP1 cause DYT6 dystonia, a childhood-onset motor disorder. DYT6 subjects display abnormalities in the white matter regions of the brain.
Here, we generated conditional THAP1 knockout mice and analyzed the gene expression profiles from motor regions of mice brains to identify a role for THAP1 in the control of myelination

overall_design: 4 WT mice, 4 Conditional THAP1 knockout mice

first: Dhananjay

last: Yellajoshyula

first: William

last: Dauer

first: Mark

last: Cookson


title: Hippocampal lipidome and transcriptome profiling alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation

city: New York

first: Prokopios Alexandros

last: Polyzos

address: 413 E 69th St

institute: Weill Cornell Medicine

summary: The widespread use of wireless devices during the last decades is rising the concern about the adverse health effects of the radiofrequency electromagnetic radiation (RF-EMR) emitted from these devices. Studies are targeting on unrevealing the underlying mechanisms of RF-EMR action. The contribution of the “omics” high throughput approaches is a prerequisite towards this direction. In the present work, C57BL/6 adult male mice were sham-exposed (nSE=8) or whole-body exposed (nExp=8) for 2h to GSM 1800 MHz mobile phone radiation at 11 V/m average electric field intensity, and the RF-EMR effects on the hippocampal lipidome and transcriptome profile were evaluated. The data analysis of the phospholipids’ fatty acid residues revealed that the levels of six fatty acids (16:0, 16:1 6+7c, 18:1 9c, 20:5 w3, SFA, MUFA) were significantly altered (p<0.05) in the exposed group. The microarray data analysis demonstrated that the expression of 178 genes changed significantly (p<0.05) between the two groups with a fold change cut off of 1.5. In general, the observed changes point out the attention to a membrane remodeling response of the tissue phospholipids after non-ionizing radiation exposure, reducing the Saturated Fatty Acids (SFA) and EPA omega-3 (20:5 w3) and increasing Monounsaturated Fatty Acids (MUFA) residues and in parallel reflect an impact to genes implicated in critical biological processes, as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism and cancer

overall_design: Mice were equally divided into two groups: “exposed” (Exp) and “sham exposed” (SE). RNA was extracted from the hippocampus of both groups.

first: Adamantia

middle: F

last: Fragopoulou

first: Lukas

last: Margaritis

first: Alexandros


title: Gene expression profiling of dendritic cells (DCs) in antibiotic-treated mice

city: Chicago

first: Yuk Man

last: Lei

state: IL

institute: University of Chicago

summary: Analysis of gene expression in DCs from peripheral lymph node (LN) of antibiotic-treated mice

overall_design: Total RNA were isolated from DCs of mice treated with broad-spectrum antibiotics for 10 days. DCs were isolated and FACS-sorted before RNA isolation

first: Yuk

first: Maria-Luisa

last: Alegre


title: Mediator 1 deficiency enhances epidermal cell fate and accelerates injury induced epidermal regeneration

status: Public on Jun 30 2017

city: San Francisco

first: Yuko

last: Oda

state: CA

address: 111N-MB 360 1700 Owens St, Suite 360

department: Endocrine Research

institute: VA Medical Center UCSF

summary: Cell fates are defined by specific transcriptional program. Previously, we developed a unique stem cell regeneration mouse model, in which transcriptional program for ectoderm organs such as tooth and skin is switched. Genomic deletion of one subunit of Mediator complex, Med1, resulted in defective enamel regeneration, in which dental stem cells were inhibited from undergoing transcriptional program for dental fate. In stead, they exerted skin program for both hair and epidermis, and post-natally regenerate ectopic hairs in the incisors. Here, we report that Med1 also modulates epidermal and hair cell fates in the skin. Med1 ablation further enhanced epidermal and sebocyte fates, and accelerated injury induced epidermal regeneration. However, it blunted hair fate resulting in hair loss in the skin. Ablation of Med1 increased the number of isthmus stem cells and epidermal stem cells, which regenerate epidermis during cutaneous wound healing process. Med1 deficiency also constitutively activated these stem cells and increased their proliferation. Microarray profiling indicated that Med1 deletion causes activation of β-catenin and suppression of TGFβ signaling. Med1 deficiency induced the expression of β-catenin target genes to control cell fate and proliferation. It also decreased TGFβ expression in interfollicular epidermis. Med1 deficiency increased the proliferation and migration of epidermal cells, and induced nuclear translocation of β-catenin, and decreased TGFβ1 expression in vitro. Our finding together with previous observations demonstrated that Med1 governs ectoderm cell fate in both tooth and skin. Med1 ablation blunts hair fate but induces epidermal and sebocyte cell fates to accelerated injury induced epidermal regeneration in the skin. Accelerated regeneration is derived from constitutive activation of epidermal stem cells accompanied with increased proliferation and migration of their progeny by balancing of β-catenin induced growth promoting and TGFβ mediated growth inhibitory activities in the skin.

overall_design: Keratinocytes were isolated from whole skin of conditional Med1knockout (cKO) mice Krt14 driven with Cre, and from no cre littermate control (CON) skin (3 mice each), and they are combined and FACS sorted by antibodies against CD34 and integrin alpha6 (a6). The CD34 negative and a6 positive population was isolated and total RNA was purified.

first: Thai

last: Nguyen

first: Daniel

last: Bikle


title: Transcriptional regulatory networks underlying reprogramming of spermatogonial stem cells (SSCs) to multipotent stem cells

status: Public on Jun 13 2017

first: Bhin

last: Jin-hyuk

address: Ji-gok research center, hyoja-dong, Nam-gu

department: Department of Chemical engineering

institute: POSTECH

summary: We present key transcription factors (TFs) and transcriptional regulatory networks (TRNs) delineating how they control cellular processes related to the SSC reprogramming.

overall_design: Using the SSCs, we first established intermediate SSCs (iSSCs) undergoing the transition to multipotent SSCs (mSSCs) and then generated gene expression profiles of SSCs, iSSCs, and mSSCs.

first: Daehee

last: Hwang

first: Jinhyuk

last: Bhin


title: Glycosyltransferase enzyme GCNT3 overexpression effect on SW620 colon cancer cells

status: Public on Jun 12 2017

city: MADRID

first: ROBERTO

last: MARTIN-HERNANDEZ

address: CARRETERA DE CANTOBLANCO

department: BIOINFORMATICS

institute: IMDEA FOOD

summary: In order to investigate glycosyltransferase enzyme GCNT3 function and to identify putative GCNT3 partners, regulators and/or downstream targets, we performed genomic analysis of GCNT3 overexpression in colon cancer cells. Data from three independent experiments were assayed in a whole genome microarray analysis. We compared patterns of global expression between GCNT3 and No ORF SW620 cells.

overall_design: Modulation of whole gene expression by GCNT3 was tested in SW620 cells using expression arrays (Agilent Human Gene Expression 4x44K Microarray Kit). Three replicates between GCNT3 stable overexpressed and control (No ORF) cells were performed. Ten µg of total RNA for each condition were used for RNA quality evaluation, amplification, labelling and hybridization to Agilent arrays according to the manufacturer's protocols.

first: Lara

last: Fernández

first: Roberto

last: Martín-Hernández

first: Ana

last: Ramírez de Molina


title: An autoregulatory RelB:p50 NF-κB pathway perpetuates pro-survival TNF response in multiple myeloma

city: New Delhi

first: Soumen

last: Basak

state: Delhi

address: Aruna Asaf Ali Marg

department: Infection and immunity

country: India

institute: National Institute of Immunology

summary: Pro-inflammatory cytokines were shown to promote growth and survival of cancerous cells.  TNF induced RelA:p50 NF-κB dimer via the canonical pathway is thought to link inflammation with cancer.  Integrating biochemical and computational studies we identify that deficiency of non-canonical signal transducer p100 triggers a positive autoregulatory loop, which instead perpetuates an alternate RelB:p50 containing NF-κB activity upon TNF treatment.  TNF stimulated RelB:p50 dimer is sufficient for mediating NF-κB target gene-expressions and suppressing apoptotic cellular death independent of principal NF-κB subunit RelA.  We further demonstrate that activating mutations in non-canonical NF-κB module deplete multiple myeloma cells of p100, thereby, provoking autoregulatory RelB:p50 activation.  Finally, autoregulatory control reinforces protracted pro-survival NF-κB response, albeit comprising of RelB:p50, upon TNF priming that protects myeloma cells with dysfunctional p100 from subsequent apoptotic insults.  In sum, we present evidence for positive autoregulation mediated through the NF-κB system and its potential involvement in human neoplasm.

overall_design: Total RNA isolated from biological replicate samples comprising of untreated and 6h TNF (10ng/ml) treated WT, Rela-/-Nfkb2-/- and Rela-/-Relb-/-Rel-/- MEFs were analyzed for global gene expression levels

first: Payel

last: Roy

first: Budhaditya

last: Chatterjee

first: Uday

last: Sarkar


title: Acsl4 Determines Ferroptosis Sensitivity by Shaping Cellular Lipid Composition

status: Public on Jun 01 2017

first: Sebastian

middle: Gerhard

last: Doll

address: Ingolstädter Landstraße 1

department: Institute of developmental genetics

institute: Helmholtz Zentrum München

summary: Ferroptosis is a form of regulated necrotic cell death controlled by glutathione peroxidase 4 (GPX4). At present, mechanisms that could predict sensitivity and/or resistance and that may be exploited to modulate this form of cell death are needed. We applied two independent approaches, a genome-wide CRISPR-based genetic screen and microarray analysis of ferroptosis-resistant cell lines to uncover acyl-CoA synthetase long-chain family member 4 (Acsl4) as an essential component for ferroptosis execution.

overall_design:
Analysis of ferroptosis-resistant cell lines to uncover acyl-CoA synthetase long-chain family member 4 (Acsl4) as an essential component for ferroptosis execution.
Expression data from ferroptosis-resistant cell clones and from ferroptosis-senitive parental cells

first: Bettina

last: Proneth

first: Yulia

last: Tyurina

first: Elena

last: Panzilius

first: Sho

last: Kobayashi

first: Irina

last: Ingold

first: Martin

last: Irmler

first: Johannes

last: Beckers

first: Michaela

last: Aichler

first: Axel

last: Walch

first: Holger

last: Prokisch

first: Dietrich

last: Trümbach

first: Joachim

last: Füllekrug

first: Christine

last: Scheel

first: Wolfgang

last: Wurst

first: Joel

last: Schick

first: Valerian

last: Kagan

first: José

last: Friedmann Angeli

first: Marcus

last: Conrad


title: Identification of long non coding RNAs associated with self-renewal capacity of rat neural stem cells exposed to sevoflurane

city: Fuzhou

first: Guo-lin

last: Lu

state: Fujian

address: No18 Daoshan Road Gulou District

country: China

institute: maternity and children Hospital of Fujian Province

summary: To identify the differential porfile of long non coding RNAs in neural stem cells exposed to sevoflurane compared with control gas(21% oxygen,5%CO2,),We employed the rat long non-coding RNA array as a discovery platform to identify genes with potential to regulate self-renewal capacity of  rat neural stem cells exposed to sevoflurane.

overall_design: Sevoflurane exposure induced gene expression in cultrued neural stem cells derived from hippocampus was detected at 6 hours  after exposure to 2.4%sevoflurane or control gas.Two different independent experiments were performed at 6 hours using tow samples of cultrued neural stem cells with exposure to sevoflurane or control gas.

first: Guo-Lin

first: Shi-Yuan

last: Xu


title: Selective increase in late sodium current leads to left ventricular fibrosis with ageing and both excessive hypertrophy and fibrosis with pressure overload in a knock-in murine model

city: Muenster

first: Ilaria

last: Piccini

address: Albert-Schweitzer-Campus 1

country: Germany

institute: UKM

summary: left ventricular transcriptional profile changes in a mouse model of Lqt3 Syndrome with age

overall_design: Total RNA obtained from isolated left ventricular tissue of  Scn5adelta/+ mice (n=4 12 months of age) compared to wild-type littermates (n=4 12 months of age).

first: I

first: L

last: Fabritz


title: Genome-wide gene expression analysis of BQ.Ncf1m1J mutated and BQ wild type mice during collagen induced arthritis

status: Public on May 10 2017

city: Turku

first: Outi

last: Sareila

address: Tykistökatu 6 A 4

institute: University of Turku

summary:
Whole blood and spleen tissue was collected 15 (d15) or 44 (d44) days postimmunization from mice immunized with type II collagen on day 0 and immunostimulated on day 21.
We compared the gene expression profiles of disease prone BQ.Ncf1m1J mice to that in BQ wild type mice. The samples were collected in two sets (marked I and II). The results show a pronounced interferon signature and increase in inflammatory transcripts in the BQ.Ncf1m1J mice.

overall_design: Each sample group consisted of tissues from 12 mice per genotype. RNA was isolated and globin removal was performed for all samples. The cells were not stimulated or selected ex vivo.

first: Tiina

last: Kelkka

first: Marjo

last: Linja

first: Rikard

last: Holmdahl


title: Dynamic modeling of the murine oocyte and somatic cell metabolome during follicle development

status: Public on Apr 18 2017

first: and

last: PhD

state: Illinois

address: 5841 South Maryland Avenue, MC 5032 Room AB540

department: Department of Surgery

country: USA

summary: Explore in vivo ovarian follicle transcriptomics from primordial follicles to the antral stage. Ovarian follicles were isolated from CD-1 mice. Entire ovaries were collected at post-natal day 3 and day 4 to collect primordial follicles. Primary follicles (70-90 µm in diameter), two-layered secondary follicles (100-130 µm), multi-layer secondary follicles (150‒180 µm), and pre-antral follicles (200‒300 µm) were mechanically isolated from post-natal day 10, 12, 16, and 18 ovaries, respectively. Antral follicles (400‒600 µm) were mechanically isolated from pregnant mare serum gonadotropin (PMSG)-treated mice ovaries at post-natal day 20. Follicles were then aspirated and combined per ovarian follicle maturation stage (e.g., primary, two-layered secondary). Three different samples were collected from each pooled follicular stage for transcriptomic analysis. RNA was purified and hybridized in MouseRef-8 v2.0 Expression BeadChip Kit (Illumina, San Diego, CA), as previously described (Skory, Bernabe et al., 2013).

overall_design: Study of murine ovarian follicle development from primordial to antral follicles

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