Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA573066 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Vascular smooth muscle cells contribute to heritable coronary artery disease risk and undergo complex transitions to multiple disease-related phenotypes. To investigate the genetic basis of these trajectories, we develop a dense timecourse single cell transcriptomic and epigenetic map of atherosclerosis in a murine disease model accompanied by high-plex in situ spatial data. Using temporal data and probabilistic fate modeling, we identify key transcription factors that drive cell state changes through a combination of network-based prioritization and in silico transcription factor perturbation. Parallel knockout studies of validated coronary artery disease gene Tcf21 uncover its molecular mechanisms in smooth muscle cell transition, due in part to a role regulating the transition of smooth muscle cells in the secondary heart field. Integrating the murine atlas with human coronary artery disease genetics pinpoint smooth muscle cell phenotypes that mediate disease risk, highlighting causal disease mechanisms. Together, these studies resolve atherosclerosis trajectories at single cell resolution and identify genetic causal transcriptomic and epigenomic mechanisms of coronary artery disease risk.
2026-02-27 | GSE321762 | GEO
Project description:LncVSM (AK098656) down-regulation in Vascular Smooth Muscle cells
| PRJNA308458 | ENA
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
2011-09-05 | E-GEOD-31928 | biostudies-arrayexpress
Project description:The prevalence of cardiovascular disease varies with sex, and the impact of intrinsic sex-based differences on vasculature is not well understood. Animal models can provide important insight into some aspects of human biology, however not all discoveries in animal systems translate well to humans. To explore the impact of chromosomal sex on proteomic phenotypes, we used iPSC-derived vascular smooth muscle cells from healthy donors of both sexes to identify sex-based proteomic differences and their possible effects on cardiovascular pathophysiology. Our analysis confirmed that differentiated cells have a proteomic profile more similar to healthy primary aortic smooth muscle than iPSCs. We also identified sex-based differences in iPSC-derived vascular smooth muscle in pathways related to ATP binding, glycogen metabolic process, and cadherin binding as well as multiple proteins relevant to cardiovascular pathophysiology and disease. Additionally, we explored the role of autosomal and sex chromosomes in protein regulation, identifying that proteins on autosomal chromosomes also show sex-based regulation that may affect the protein expression of proteins from autosomal chromosomes. This work supports the biological relevance of iPSC-derived vascular smooth muscle cells as a model for disease, and further exploration of the pathways identified here can lead to the discovery of sex-specific pharmacological targets for cardiovascular disease.
2024-07-23 | MSV000095417 | MassIVE
Project description:LncVSM (AK098656) up/down-regulation in Vascular Smooth Muscle cells
| PRJNA305751 | ENA
Project description:Global effects of 2-methoxyestradiol on smooth muscle cell hyperproliferation and vascular remodeling in atherosclerosis
| PRJNA113643 | ENA
Project description:Smooth muscle cells (SMCs) are important in a number of physiological systems and organs, including the cardiovascular system. The hallmark property of differentiated SMCs is the ability to contract, but contractile SMCs themselves show a range of phenotypes allowing prolonged tonic contraction in vascular smooth muscle or rapid phasic contraction in tissues such as bladder. Another distinctive characteristic, in contrast with terminally differentiated striated muscle cells, is that SMCs exhibit phenotypic plasticity. Vascular SMCs are able to modulate their phenotype along a continuum between a contractile phenotype, characteristic of healthy blood vessels, and a more proliferative âsyntheticâ phenotype, so-named for the enhanced synthesis and secretion of extracellular matrix components. Synthetic phenotype cells are found in a number of pathological situations such as atherosclerosis and arterial injury. We used mouse exon-junction (MJAY) arrays to gain insights into both the global contribution of alternative splicing events in re-shaping the transcriptome of dedifferentiating mouse aorta and bladder SMCs, and into the underlying regulatory mechanisms of the alternative splicing program. Affymetrix splice junction arrays (MJAY) were used to profile changes in both alternative splicing and transcript levels during the phenotypic modulation of smooth muscle cells when placed in culture. RNA extracted from intact aorta and bladder smooth muscle tissue was used for differentiated samples. For dedifferentiated, proliferative samples smooth muscle cells were enzymatically dispersed and grown in tissue culture for a week. Triplicate RNA samples were prepared from smooth muscle tissue of mouse aorta and bladder (differentiated) and from smooth muscle cells from each tissue cultured for 7 days (proliferative). The samples allowed comparison of alternative splicing (and other transcriptome) changes between differentiated and proliferative smooth muscle cell samples from two distinct types of smooth muscle cell, as well as allowing direct comparison of aorta (tonic smooth muscle) and bladder (phasic smooth muscle).
2016-07-01 | E-MTAB-4841 | biostudies-arrayexpress
Project description:Vascular smooth muscle cells (VSMCs) are derived from distinct embryonic origins. Vessels originating from differing smooth muscle cell populations have distinct vascular and pathological properties of calcification, atherosclerosis, and structural defects such as aneurysm and coarctation. We hypothesized that domains within a vessel vary in phenotype based on embryonic origin. We used microarrays to detail the expression differences in vasculature of different embryonic origin. Mouse tissues were selected from different vascular compartments for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify embryonic origin-specific expression profiles.
2014-08-26 | E-GEOD-50250 | biostudies-arrayexpress
Project description:Vascular smooth muscle cells (VSMCs) are derived from distinct embryonic origins. Vessels originating from differing smooth muscle cell populations have distinct vascular and pathological properties of calcification, atherosclerosis, and structural defects such as aneurysm and coarctation. We hypothesized that domains within a vessel vary in phenotype based on embryonic origin. We used microarrays to detail the expression differences in vasculature of different embryonic origin. Mouse tissues were selected from different vascular compartments for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify embryonic origin-specific expression profiles.
2014-08-26 | E-GEOD-50251 | biostudies-arrayexpress
Project description:The deubiquitinase USP17 was previously shown to regulate KLF4 expression in hepatocellular carcinomas. The KLF4 transcription factor is a major regulator of the phenotypic response of vascular smooth muscle cells, enabling their polarization toward a synthetic phenotype observed in several aortic remodeling diseases, including aneurysms and atherosclerosis. The aim here was therefore to reduce USP17 expression in primary-cultured human aortic smooth muscle cells and to verify their fate (contractile or synthetic phenotype) through proteomic analysis.
2026-02-25 | PXD074824 | Pride