Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PARP1 regulates VSMC phenotypic switch and neointima via Myocardin

ABSTRACT: We applied the transcriptome profiling (RNA-seq) for high-throughput profiling of genes changes in VSMC dedifferentiation. Rat primary VSMCs were divided into 3 groups, control, PDGF-BB, PDGF-BB+PJ34,and mRNA sequence were performed. We found that PDGF-BB could upregualted the genes involved in cell proliferation and migration, and downregulated the VSMC contractile genes, all of which could be reversed by PARP inhibitor PJ34. Then we knockdowned the co-factor Myocardin in VSMCs, and found the above effects of PJ34 were nearly abolished.Our study first provided the transcription changes by RNA-seq in VSMC dedifferentiation, and demonstrated the key roles of PARP1 and the PARylation process in VSMC phenotypic switch.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE103995 | GEO | 2018/09/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Disfunction of arachidonic acid metabolism in vascular smooth muscle cells contributes to restenosis

Project description:We applied the transcriptome profiling (RNA-seq) for high-throughput profiling of genes changes in the phenotypic switch of VSMCs. Rat primary VSMCs were divided into 3 groups, control, PDGF-BB, PDGF-BB+PTUPB,and mRNA sequence were performed. We found that Cell cycle related genes and cellular senescence related genes were significantly upregulated by PDGF-BB and significantly reversed by PTUPB. Subsequently, we deleted PTTG1 as a key gene for PTUPB to reverse phenotypic switching in VSMCs. Our study provided the transcription changes by RNA-seq in VSMC phenotypic switch, and found that PTUPB played a crucial role in correcting the dysregulation of sEH/COX-2 derived ARA metabolism in VSMC phenotypic switch

2023-09-01 | GSE241545 | GEO

The THO Complex-Dependent Posttranscriptional Control Contributes to Vascular Smooth Muscle Cell Fate Decision

Project description:We applied RNA-Seq to analyze the effects of silencing of Thoc2 or Thoc5, two components of the THO complex, in cultured VSMC. The result revealed that Thoc5 silencing closely resembled the gene expression changes induced upon PDGF-BB/PDGF-DD treatments in cultured VSMCs. Mechanistically, our RIP-Seq data revealed both Thoc2 and Thoc5 preferentially interacted with VSMC marker gene mRNAs and mediated their expression. Interestingly, mRNAs that lost Thoc2 or Thoc5 binding during VSMC dedifferentiation were enriched for genes important for VSMC identity. In addition, silencing of Thoc2 or Thoc5 led to dedifferentiation of VSMCs in vitro, characterized by decreased VSMC marker gene expression and increased migration and proliferation. Furthermore, we performed immuno-histochemical staining against Thoc2 and Thoc5, and found a dramatic reduction in their expression in human arteries undergoing carotid endarterectomy (CEA) compared to normal internal mammary arteries (IMA). Notably, Thoc5 overexpression in injured rat carotid arteries significantly repressed loss of VSMC marker gene expression and neointima formation. Together, our data introduce dynamic binding of THO to VSMC marker gene mRNAs as a novel mechanism contributing to VSMC fate decisions, and imply Thoc5 as a potential intervention node for vascular diseases.

2018-12-06 | GSE116850 | GEO

Thymosin 4 protects against aortic aneurysm via endocytic regulation of growth factor signalling

Project description:Vascular stability and tone are maintained by contractile smooth muscle cells (VSMCs). However, injury-induced growth factors stimulate a contractile-synthetic phenotypic modulation which increases susceptibility to abdominal aortic aneurysm (AAA). As a regulator of embryonic VSMC differentiation, we hypothesised that Thymosin β4 (Tβ4) may function to maintain healthy vasculature throughout postnatal life. This was supported by the identification of an interaction with Low density lipoprotein receptor related protein 1 (LRP1), an endocytic regulator of PDGF-BB signalling and VSMC proliferation. LRP1 variants have been implicated by genome-wide association studies with risk of AAA and other arterial diseases. T4-null mice displayed aortic VSMC and elastin defects, phenocopying LRP1 mutants, and their compromised vascular integrity predisposed to Angiotensin II-induced aneurysm formation. Aneurysmal vessels were characterised by enhanced VSMC phenotypic modulation and augmented platelet-derived growth factor (PDGF) receptor (PDGFR)β signalling. In vitro, enhanced sensitivity to PDGF-BB, upon loss of Tβ4, associated with dysregulated endocytosis, with increased recycling and reduced lysosomal targeting of LRP1-PDGFRβ. Accordingly, the exacerbated aneurysmal phenotype in T4-null mice was rescued upon treatment with the PDGFRβ antagonist, Imatinib. Our study identifies Tβ4 as a key regulator of LRP1 for maintaining vascular health and provides insights into the mechanisms of growth factor-controlled VSMC phenotypic modulation underlying aortic disease progression.

2021-05-21 | PXD024162 | Pride

PARP1 regulates VSMC phenotypic switch and neointima via Myocardin

Project description:PARP1 regulates VSMC phenotypic switch and neointima via Myocardin

| PRJNA407927 | ENA

Rat vascular smooth muscle cells LC-MS/MS

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

VSMC gene in normal kdney and chronic kidney mice

Project description:Analysis of RNAs from VSMCs to find altered pathways in VSMC by CKD

2024-04-08 | GSE229679 | GEO

Microarray expression profile and bioinformatics analysis of circular RNAs in the phenotypic switching of rat vascular smooth muscle cells: a preliminary study

Project description:In order to further study the role of circular RNA in the phenotypic transformation of vascular smooth muscle cells (VSMCs), the differential expression profile of circRNA in the phenotypic transition of VSMCs induced by platelet-derived growth factor-BB (PDGF-BB) was screened using chip technology. Vascular smooth muscle cells from rat thoracic aorta were induced with 20ng/ml PDGF-BB as the experimental group and compared with the control group. After induction for 24 hours, the differentially expressed circRNA was screened by circular RNA chip.

2021-12-17 | GSE190952 | GEO

Role of ZHX2 in VSMCs [RNA-seq]

Project description:Primary rat VSMCs were infected with Ad-Control and Ad-ZHX2 and stimulated with PDGF-BB of 24h. RNAseq and differential expression analysis were performed to investigate the role of ZHX2 in VSMCs.

2023-10-07 | GSE244564 | GEO

Microassay analysis of the lncRNAs expression profile in human aortic vascular smooth muscle cells(hAoSMCs) treated with PDGF-BB at 24 h.

Project description:Atherosclerosis is the most important mechanism of cardiovascular and cerebrovascular diseases and has become one of the most serious diseases that threaten human health. Vascular smooth muscle cells (VSMCs) are the main cellular components that constitute the structure of the blood vessel wall. The excessive proliferation and migration are pivotal pathological basis of atherosclerosis, in-stent restenosis, pulmonary hypertension and other vascular proliferative diseases. PDGF-BB is a potent proliferative agent for VSMCs, but the specific mechanism of PDGF-BB signaling pathway involved in biological processes such as proliferation and migration of VSMCs is not elusive.

2023-10-22 | GSE186313 | GEO

Angiotensin II regulated gene expression in rat primary vascular smooth muscle cells (VSMC)

Project description:Atherosclerosis is one of the causative factors leading to the development of cardiovascular disease. Angiotensin II (AngII) is implicated in the pathological processes underlying atherosclerosis. We investigated the AngII regulated gene expression in primary vascular smooth muscle cells (VSMC). VSMCs were isolated from the thoracic aorta of male Wistar rats. Serum deprived VSMCs were stimulated with 100 nM AngII or vehicle for 2 hours, then RNA-Sequencing was carried out.

2022-07-03 | E-MTAB-11863 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data