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Genome wide analysis of genes expressed in early G1 phase of the cell cycle in PMCA4 wild type and PMCA4 knockout primary vascular smooth muscle cells

ABSTRACT: Husain lab cell proliferation in vitro experimental data showed a G1 arrest in PMCA4 knockout primary vascular smooth muscle cells (VSMC). This microarray documents the different gene expression profiles of PMCA4 wild type and knockout cells at the early G1 stage in serum synchronized cell populations (n=4 populations for each genotype).

ORGANISM(S): Mus musculus

PROVIDER: GSE38318 | GEO | 2014/01/21

SECONDARY ACCESSION(S): PRJNA167714

REPOSITORIES: GEO

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Genome wide analysis of genes expressed in early G1 phase of the cell cycle in PMCA4 wild type and PMCA4 knockout primary vascular smooth muscle cells

Project description:Husain lab cell proliferation in vitro experimental data showed a G1 arrest in PMCA4 knockout primary vascular smooth muscle cells (VSMC). This microarray documents the different gene expression profiles of PMCA4 wild type and knockout cells at the early G1 stage in serum synchronized cell populations (n=4 populations for each genotype). Serum synchronized cell populations were Hoechst labeled and flow sorted for early G1 sub-populations (PMCA4 WT n=4; PMCA4 KO n=4) and total RNA from sorted cells was used for microarray analysis.

2014-01-21 | E-GEOD-38318 | biostudies-arrayexpress

Genome wide analysis of genes expressed in late G1/S phase of the cell cycle in PMCA4 knockout (P4KO) and P4KO rescued with PMCA4a primary vascular smooth muscle cells

Project description:Husain lab cell proliferation in vitro experimental data showed that electroporating PMCA4a cDNA into P4KO cells rescued the G1 arrest phenotype in P4KO primary vascular smooth muscle cells (VSMC). This microarray documents the different gene expression profiles of P4KO and P4KO+PMCA4a VSMC at the late G1/S stage in serum synchronized cell populations (n=4 populations for each genotype).

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Genome wide analysis of genes expressed in late G1/S phase of the cell cycle in PMCA4 knockout (P4KO) and P4KO rescued with PMCA4a primary vascular smooth muscle cells

2014-01-21 | E-GEOD-46744 | biostudies-arrayexpress

Genome wide analysis of genes expressed in late G1/S phase of the cell cycle in PMCA4 wild type (P4WT), PMCA4 knockout(P4KO), P4KO rescued with PMCA4b and P4KO rescued with Vector primary vascular smooth muscle cells

Project description:Husain lab cell proliferation in vitro experimental data showed that electroporating PMCA4b cDNA into P4KO cells rescued the G1 arrest phenotype in P4KO primary vascular smooth muscle cells (VSMC). This microarray documents the different gene expression profiles of P4WT, P4KO, P4KO+PMCA4b and P4KO+Vector VSMC at the late G1/S stage in serum synchronized cell populations (n=4 or 5 populations for each genotype).

2014-01-21 | GSE38319 | GEO

2014-01-21 | E-GEOD-38319 | biostudies-arrayexpress

To examine vascular smooth muscle cells (VSMC) under four conditions

Project description:Vascular calcification is a hallmark of atherosclerosis and end-stage renal disease (ESRD). However, the molecular mechanism of vascular calcification is poorly understood. Diabetes mellitus is increasingly recognized as the most important cause for atherosclerosis and ESRD. Emerging evidence supports the concept that vascular calcification resembles the process of osteogenesis, in which the vascular smooth muscle cells (VSMC) undergo osteochondrogenic differentiation. Recently, we have established an in vitro calcification system with primary mouse VSMC. With the use of osteogenic stimuli, we induced trans-differentiation of primary mouse VSMC into bone-like cells. Interestingly stroptozotocin (STZ), O-GlcNAcase inhibitor and a drug that has been used to induce diabetes in mice, was able to induce calcification of VSMC and the expression of the osteogenic transcription factor Runx2, suggesting glycosylation may be involved in regulation of Runx2. We have reported an essential role of Runx2 in oxidative stress-induce VSMC calcification and have recently generated a tissue specific mouse with Runx2 ablation in smooth muscle cells. Therefore, we will use STZ and other relevant reagents in the glucose synthesis/metabolism pathways as stimuli for VSMC calcification to characterize the glycogene profiles during VSMC calcification. Results from VSMC of Runx2 knockout mice will be compared with those from control mice to determine the regulation of calcification-associated glycogenes by Runx2 in response to STZ. These studies will provide foundation for further mechanistic studies and may lead to identification of novel strategies and targets for diabetes-induced vascular calcification. To examine vascular smooth muscle cells (VSMC) under two conditions: 1) wild-type VSMC differentiated into bone-like cells with osteogenic media, 2) wild-type VSMC treated with STZ and osteogenic media

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Heterogeneous Expression of Alternatively Spliced lncRNA mediates Vascular Smooth Cell Plasticity

Project description:9p21 locus polymorphisms have the strongest correlation with coronary artery disease, but as a non-coding locus, disease connection is enigmatic. The lncRNA ANRIL found in 9p21 may regulate vascular smooth muscle cell (VSMC) phenotype to contribute to disease risk. We observed significant variability in induced pluripotent stem cell-derived VSMCs from patients homozygous for risk versus isogenic knockout or non-risk haplotypes. Sub-populations of risk haplotype cells exhibited variable morphology, proliferation, contraction, and adhesion. When sorted by adhesion, risk VSMCs parsed into synthetic and contractile sub-populations, i.e., weakly adherent and strongly adherent, respectively. >90% of differentially expressed genes co-regulated by haplotype and adhesion were associated with Rho GTPases, i.e., contractility. Weakly adherent sub-populations expressed more short isoforms of ANRIL, and when overexpressed in knockout cells, ANRIL suppressed adhesion, contractility, and αSMA expression. These data are the first to suggest that variable lncRNA penetrance may drive mixed functional outcomes that confound pathology.

2022-08-19 | GSE211144 | GEO

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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.

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Proteomic Profiling Exosomes from Vascular Smooth Muscle Cell

Project description:The components of the exosomes are essential to understand how vascular smooth muscle cells (VSMC) and endothelial cells communicate with each other. Exosomes secreted by human VSMCs were harvested and analyzed by nanoLC-MS/MS. The activity of the identified proteins were further assessed by the in vivo matrigel plug angiogenesis assay.

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AngII-regulated genes sensitive to CsA in Vascular Smooth muscle cells.

Project description:We have employed whole genome microarray expression profiling as a platform to identify AngII -regulated genes sensitive to CsA. VSMC were treated with AngII with or without CsA ( as an inhibitor of the CN/NFAT pathway). 4 independent VSMC cultures (4 replicates) from aortas of C57BL/6 mice were used for each condition (1uM AngII or 1uM AngII+200ng/ml CsA).

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