Histone 3 Lysine 9 Dimethylation Attenuates the Vascular Smooth Muscle Cell Inflammatory Response
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ABSTRACT:
PROVIDER: PRJNA542913 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9054680_1.fastq.gz | Fastqsanger.gz | |||
| SRR9054680_2.fastq.gz | Fastqsanger.gz | |||
| SRR9054681_1.fastq.gz | Fastqsanger.gz | |||
| SRR9054681_2.fastq.gz | Fastqsanger.gz | |||
| SRR9054682_1.fastq.gz | Fastqsanger.gz |
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Project description:Vascular inflammation underlies cardiovascular disease. Vascular smooth muscle cells (VSMCs) upregulate selective genes, including matrix metalloproteinases (MMPs) and pro-inflammatory cytokines in response to local inflammation, which directly contribute to vascular disease and adverse clinical outcome. Identification of factors controlling VSMC responses to inflammation is therefore of considerable therapeutic importance. Here, we determine the role of H3K9me2, a repressive epigenetic mark that is reduced in atherosclerotic lesions, in regulating the VSMC inflammatory response. We used VSMC-lineage tracing to detect reduced H3K9me2 levels in VSMCs of arteries after injury and in atherosclerosis. Intriguingly, chromatin immunoprecipitation revealed H3K9me2 enrichment at a subset of inflammation-responsive gene promoters, including MMP3, MMP9, MMP12 and IL6, in mouse and human VSMCs. Inhibition of G9A/GLP, the primary enzymes responsible for H3K9me2, significantly potentiated inflammation-induced gene induction in vitro and in vivo without altering NFkB and MAPK signalling. Rather, reduced G9A/GLP activity enhanced inflammation-induced binding of transcription factors NFkB-p65 and cJUN to H3K9me2 target gene promoters MMP3 and IL6. Taken together, these results suggest that promoter-associated H3K9me2 directly attenuates the induction of target genes in response to inflammation in human VSMCs. This study implicates H3K9me2 in regulating the pro-inflammatory VSMC phenotype. Our findings suggest that reduced H3K9me2 in disease allows complete binding of NFkB and AP-1 transcription factors at specific inflammation-responsive genes to augment pro-inflammatory stimuli in VSMC. Since increased MMP and IL6 activity are features of vascular disease, H3K9me2-regulation may be a novel target for clinical intervention.
2019-12-05 | GSE131212 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE29146: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [ChIP] GSE29147: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi] GSE29148: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO] GSE29150: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [Transduction] Refer to individual Series
2011-11-29 | E-GEOD-29305 | biostudies-arrayexpress
Project description:Normal cell type specific histone H3 lysine 9 dimethylation of miRNA genes. HMEC and HMF represent two distinct differentiated cell type present in mammary gland each with a distinct phenotype, a distinct epigenotype as well as distinct miRNA expression pattern. The aim of the study was to determine how epigenetic modifications including histone H3 lysine 9 dimethylation affect miRNA expression. Two cell types HMEC vs. HMF. Biological replicates: 3 pairs of HMEC-HMF of 3 distinct genotypes. Immunoprecipitation using anti-histone H3 dimethylated at lysine 9 (CS200587, Millipore).
2011-04-05 | E-GEOD-28378 | biostudies-arrayexpress
Project description:Normal cell type specific histone H3 lysine 9 dimethylation of miRNA genes. HMEC and HMF represent two distinct differentiated cell type present in mammary gland each with a distinct phenotype, a distinct epigenotype as well as distinct miRNA expression pattern. The aim of the study was to determine how epigenetic modifications including histone H3 lysine 9 dimethylation affect miRNA expression.
2011-04-05 | GSE28378 | GEO
Project description:ObjectiveVascular inflammation underlies cardiovascular disease. Vascular smooth muscle cells (VSMCs) upregulate selective genes, including MMPs (matrix metalloproteinases) and proinflammatory cytokines upon local inflammation, which directly contribute to vascular disease and adverse clinical outcome. Identification of factors controlling VSMC responses to inflammation is therefore of considerable therapeutic importance. Here, we determine the role of Histone H3 lysine 9 di-methylation (H3K9me2), a repressive epigenetic mark that is reduced in atherosclerotic lesions, in regulating the VSMC inflammatory response. Approach and Results: We used VSMC-lineage tracing to reveal reduced H3K9me2 levels in VSMCs of arteries after injury and in atherosclerotic lesions compared with control vessels. Intriguingly, chromatin immunoprecipitation showed H3K9me2 enrichment at a subset of inflammation-responsive gene promoters, including MMP3, MMP9, MMP12, and IL6, in mouse and human VSMCs. Inhibition of G9A/GLP (G9A-like protein), the primary enzymes responsible for H3K9me2, significantly potentiated inflammation-induced gene induction in vitro and in vivo without altering NFκB (nuclear factor kappa-light-chain-enhancer of activated B cell) and MAPK (mitogen-activated protein kinase) signaling. Rather, reduced G9A/GLP activity enhanced inflammation-induced binding of transcription factors NFκB-p65 and cJUN to H3K9me2 target gene promoters MMP3 and IL6. Taken together, these results suggest that promoter-associated H3K9me2 directly attenuates the induction of target genes in response to inflammation in human VSMCs.ConclusionsThis study implicates H3K9me2 in regulating the proinflammatory VSMC phenotype. Our findings suggest that reduced H3K9me2 in disease enhance binding of NFκB and AP-1 (activator protein-1) transcription factors at specific inflammation-responsive genes to augment proinflammatory stimuli in VSMC. Therefore, H3K9me2-regulation could be targeted clinically to limit expression of MMPs and IL6, which are induced in vascular disease.
| S-EPMC6818986 | biostudies-literature
Project description:The full length of LncVSM transfected into Vascular Smooth Muscle cells to down-regulation for screening differential expression prolifes of LncVSM effecting.The empty vector transfected Vascular Smooth Muscle cells as controls. Eight Samples analyzed.
2016-01-12 | E-GEOD-76720 | biostudies-arrayexpress
Project description:YAP/TAZ in vascular smooth muscle
| PRJNA610067 | ENA
Project description:Crotonylation of histones is discovered of late as one of post-translational modification that can regulate gene expression. However, the function of crotonylation on non-histone proteins in vascular smooth muscle cells (VSMC) is unclear. Here, we aim to use modification and proteomic analysis to find the cellular characteristic of crotonylated non-histone proteins and the crosstalk with ubiquitinated proteins in vascular smooth muscle cell (VSMC) phenotypic remodeling. We performed modification and proteomic analysis of VSMCs before and after stimulated with platelet-derived growth factor-BB (PDGF-BB). The crotonylated and ubiquitinated pan-antibody was used to enrich the protein and then subjected to high-throughput mass spectrometry analysis. The enrichment analysis was performed within differentially modified proteins in regards to GO terms, KEGG and protein domain.
2022-05-19 | PXD029070 | Pride
Project description:Investigation of the physiogical functions of YAP/TAZ in vascular smooth muscle cells
2020-11-16 | GSE146317 | GEO
Project description:The full length of LncVSM transfected into Vascular Smooth Muscle cells to down-regulation for screening differential expression prolifes of LncVSM effecting.The empty vector transfected Vascular Smooth Muscle cells as controls.
2016-01-12 | GSE76720 | GEO