GEO Logo
   NCBI > GEO > Accession DisplayHelp Not logged in | LoginHelp
GEO help: Mouse over screen elements for information.
Series GSE143148 Query DataSets for GSE143148
Status Public on Jan 08, 2020
Title The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition [HTS]
Organisms Homo sapiens; Mus musculus
Experiment type Expression profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
Summary Endothelial cells play an important role in maintenance of the vascular system and the repair after injury. Under pro-inflammatory conditions, endothelial cells can acquire a mesenchymal phenotype by a process named endothelial-to-mesenchymal transition (EndMT), which affects the functional properties of endothelial cells. Here, we investigated the epigenetic control of EndMT. We show that the histone demethylase JMJD2B is induced by EndMT promoting pro-inflammatory and hypoxic conditions. Silencing of JMJD2B reduced TGF-β2-induced expression of mesenchymal genes and prevented the alterations in endothelial morphology and impaired endothelial barrier function. Endothelial-specific deletion of JMJD2B in vivo confirmed a reduction of EndMT after myocardial infarction. EndMT did not affect global H3K9me3 levels but induced a site-specific reduction of repressive H3K9me3 marks at promoters of mesenchymal genes, such as Calponin (CNN1), and genes involved in TGF-β signaling, such as AKT Serine/Threonine Kinase 3 (AKT3) and sulfatase 1 (SULF1). Silencing of JMJD2B prevented the EndMT-induced reduction of H3K9me3 marks at these promotors and further repressed these EndMT-related genes. Our study reveals that endothelial identity and function is critically controlled by the histone demethylase JMJD2B, which is induced by EndMT-promoting pro-inflammatory and hypoxic conditions and support the acquirement of a mesenchymal phenotype.
Overall design 1.) CHIP-SEQ of H3K9me3 in HUVECS in full-(FM) and differentiation medium (DM)
2.) Whole Transcriptome RNA-SEQ of HUVECS in full-(FM) and differentiation medium (DM)
3.) Single Cell RNA-SEQ of whole heart of Jmjd2b flox Cdh5-iCre and wildtype mice 3 days after AMI
4.) Single Cell RNA-SEQ of HUVECS full-(FM) and differentiation medium (DM)
5.) Single Cell RNA-SEQ of HUVECS in full medium (FM) under scrambled knockdown and differentiation medium (DM) under scrambled knockdown and JMJD2B knockdown
Contributor(s) Glaser SF, Dimmeler S
Citation(s) 32034099
Submission date Jan 06, 2020
Last update date Apr 08, 2020
Contact name David John
Organization name Institute for Cardiovascular Regeneration
Street address Theodor-Stern-Kai 7
City Frankfurt
State/province Hessen
ZIP/Postal code 60590
Country Germany
Platforms (3)
GPL18573 Illumina NextSeq 500 (Homo sapiens)
GPL24247 Illumina NovaSeq 6000 (Mus musculus)
GPL24676 Illumina NovaSeq 6000 (Homo sapiens)
Samples (27)
GSM4254146 HUVEC_DM_n1 [RNA-seq]
GSM4254147 HUVEC_DM_n2 [RNA-seq]
GSM4254148 HUVEC_DM_n3 [RNA-seq]
This SubSeries is part of SuperSeries:
GSE143151 The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition
BioProject PRJNA599372
SRA SRP239802

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE143148_Gene_expression.tsv.gz 3.0 Mb (ftp)(http) TSV
GSE143148_RAW.tar 780.0 Kb (http)(custom) TAR (of BED)
GSE143148_inVitro_FM-vs_EndMT_Expressionmatrix.csv.gz 104.5 Mb (ftp)(http) CSV
GSE143148_inVitro_siScr_vs_siJMJD2B_EndMt_FM_Expressionmatrix.csv.gz 156.9 Mb (ftp)(http) CSV
GSE143148_inVivo_Expressionmatrix.csv.gz 103.3 Mb (ftp)(http) CSV
SRA Run SelectorHelp
Raw data are available in SRA
Processed data are available on Series record
Processed data provided as supplementary file

| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap