Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA sequencing of porcine smooth muscle cells, after treatments with platelet derived growth factor and S100A4 protein

ABSTRACT: Smooth muscle cells were treated with platelet derived growth factor (PDGF-BB) and S100A4 protein to decipher the mechanisms by which they contribute to smooth muscle cell phenotypic transition. We report that PDGF-BB treatment upregulates genes related to growth response or to extracellular matrix component proteases, while S100A4 upregulates pro-inflammatory genes. When used in combination, PDGF-BB and S100A4 show synergistic action by enhancing the upregulation of genes already affected by S100A4 and by inducing the upregulation of genes exclusive for this condition.

ORGANISM(S): Sus scrofa

PROVIDER: GSE143296 | GEO | 2022/01/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiling regulated by PDGF in pBSMCs

Project description:To explore global molecular changes in smooth muscle in response to PDGFR activation, primary human bladder smooth muscle cells were treated with 1 nM PDGF-BB (hereafter PDGF) for 0, 4 or 24 h. Total RNA were prepared, and analyzed using expression profiling, and subjected to bioinformatic and functional interrogation. To identify molecular signatures of bladder smooth muscle peturbed by PDGF, primary human bladder smooth muscle cells were treated with 1 nM PDGF-BB (hereafter PDGF) for 0, 4 or 24 h.

2014-10-06 | E-GEOD-52488 | biostudies-arrayexpress

Gene expression in occlusive vein grafts following CABG of human

Project description:To further understand the mechanism approach to occlusive vein grafts, we have employed RNA-seq to identify key genes in occlusive venin grafts following CABG in human. The occluded vein graft and intraoperative spare great saphenous vein of patients undergoing clinical re-coronary artery bypass grafting were obtained for RNA-seq. The sequencing results were cleaned and bioinformatics annlysis was conducted by using WGCNA and a variety of online databases and software. The key genes or proteins affecting the occurrence of vein graft restenosis were screened out(ITGB2), and the expression level of the target genes or proteins was verified by real-time PCR and Western blot. And to further learn the effect of ITGB2 in human primary venous smooth muscle cells, ITGB2 gene was silenced by SiRNA. The effect of ITGB2 silencing on proliferation, migration and invasion of venous smooth muscle cells after PDGF-BB-stimulation were detected by Edu assay, scrathch experiment and transwell experiment. And Edu assay showed that ITGB2 silencing could inhibit the proliferation of PDGF-BB sitmulated smooth muscle cells. Scratch assay showed that ITGB2 silencing inhibited the migration of PDGF-BB stimulated smooth muscle cells. Transwell assay showed that ITGB2 silencing significantly inhibited the invasion of PDGF-BB stimulated smooth muscle cells. It is indicated that ITGB2 was the key gene in vein graft restenosis,and may be the potential treatment target in restenosis patients.

2024-01-17 | GSE241205 | GEO

Small RNA profiling of differentiated and de-differentiated vascular smooth muscle cell

Project description:We report the application of small RNA sequencing for high-throughput profiling of small RNA under 75 bp in vascular smooth muscle cell. By a reading depth of 30M and single stranded sequencing, we generated the small RNA signature on differentiated and de-differentiated vascular smooth muscle cell induced by PDGF-BB and H3K4me2 editing. We found that PDGF-BB and H3K4me2 editing induced de-differentiation modulated miRNA profile significantly, which was demonstrated at least in part responsible for modulated vascular smooth muscle cell phenotype.

2022-04-01 | GSE186972 | 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

Gene expression profiling regulated by PDGF in pBSMCs

2014-10-06 | GSE52488 | GEO

Genes induced by PDGF-BB in cells lacking Signal Transducer and Activator of Transcription-1 (Stat1)

Project description:Comparison of gene expression between Stat1+/- and Stat1-/- dermal fibroblasts or vascular smooth muscle cells after treatment with PDGF-BB for one hour.

2020-06-13 | GSE152342 | GEO

SILAC analysis of PDGF-treated primary bladder smooth muscle cells

Project description:SILAC analysis of human primary bladder smooth muscle cells treated with platelet-derived growth factor for 0, 4, and 24 h. Platelet-derived growth factor-BB (PDGF-BB) is a mitogen and motogen that has been implicated in the proliferation, migration and synthetic activities of smooth muscle cells (SMC) that characterize pathologic tissue remodeling in hollow organs. To explore the signals induced by PDGF on a global scale, we performed expression profiling and quantitative proteomics analysis of PDGF-treated human visceral SMC. 1695 genes and 241 proteins were identified as differentially expressed in PDGF-treated primary bladder SMC versus non-treated cells. Analysis of gene expression data revealed MYC, JUN, EGR1, MYB and RUNX1 as the transcription factors most significantly networked with upregulated genes; DDIT3, NFAT5, and SOX5 were most networked with downregulated genes. For protein identification and quantification, raw mass spectrometric data were analyzed with MaxQuant software (version 1.0.13.13). The parameters were set as follows. In the Quant module, SILAC triplets was selected; oxidation (M) and acetyl (Protein N-term) were set as variable modification; carbamidomethyl (C) was set as fixed modification; concatenated IPI human database (version 3.52) (74,190 forward sequences and 74,190 reverse sequences) was used for database searching; all other parameters were default. Tandem mass spectra were searched by Mascot (version 2.2.0.4) (Matrix Science, Boston, MA). In the Identify module, all parameters were default, except that maximal peptide posterior error probability was set as 0.05. False discovery rates for protein and peptide identifications were both set at 0.01.

2014-08-04 | PXD000624 | Pride

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

GP IIb/IIIa-ICAM-1 Mediated Platelet-Endothelial Adhesion Exacerbates Pulmonary Hypertension

Project description:Pulmonary hypertension (PH) patients typically present with a diminished platelet count, but the role of platelets in the development and progression of PH remains unclear.Transcriptomic analysis revealed that platelets from PH patients exhibited an upregulation of genes associated with cellular adhesion, platelet activation, and adhesion. Notably, the hub genes, glycoprotein IIb/IIIa (GP IIb/IIIa), were implicated in mediating platelet-endothelium adhesion through their interaction with intercellular adhesion molecule-1 (ICAM-1) on pulmonary artery endothelial cells, triggering platelet activation and the subsequent release of platelet-derived growth factor BB (PDGF-BB).

2024-12-09 | GSE283520 | GEO

Dysfunction of S100A4+ effector memory CD8+ T cells aggravates asthma

Project description:Progressive loss of effector functions, especially IFN-γ secreting capability, in effector memory CD8+ T (CD8+ TEM) cells plays a causal role in asthma worsening. However, the mechanisms of CD8+ TEM cell dysfunction remain elusive. Here, we report that S100A4 drives CD8+ TEM cell dysfunction, impairing their protective memory response and promoting asthma worsening in OVA-induced asthma model. We find that allergic CD8+ TEM cells contain two subsets based on S100A4 expression. S100A4+ subsets exhibit dysfunctional effector phenotypes with increased proliferative capability, whereas S100A4- subsets retain effector function but are more inclined to apoptosis, giving rise a dysfunctional CD8+ TEM cell pool. Mechanistically, S100A4 upregulation of mitochondrial metabolism results in a decrease of acetyl-CoA levels, which impair the transcription of effector genes, especially ifn-γ, facilitating cell survival, tolerance and memory potential. Our findings thus reveal general insights into how S100A4 reprograms CD8+ TEM cells into dysfunctional and less protective phenotypes to promote asthma worsening.

2022-03-11 | GSE162116 | GEO

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