Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bulk RNAseq Analysis of Murine Thoracic Aortas with Tsc1+/+ and Tsc1-/- Smooth Muscle Cells

ABSTRACT: We characterized the transcriptomic effects of chronic mTOR activation in aortic SMCs using a conditional genetic model to delete Tsc1 under control of a smooth muscle-specific Myh11 promoter

ORGANISM(S): Mus musculus

PROVIDER: GSE135177 | GEO | 2019/08/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Single-Cell RNAseq Analysis of Murine Fate-Mapped Tsc1+/+ and Tsc1-/- Aortic Smooth Muscle Cells

Project description:We characterized the transcriptomic effects at the single cell level of chronic mTOR activation in aortic SMCs using a conditional genetic model to delete Tsc1 under control of a smooth muscle-specific Myh11 promoter

2019-08-02 | GSE135240 | GEO

Bulk RNAseq Analysis of Murine Thoracic Aortas with Tsc1+/+ and Tsc1-/- Smooth Muscle Cells

Project description:Bulk RNAseq Analysis of Murine Thoracic Aortas with Tsc1+/+ and Tsc1-/- Smooth Muscle Cells

| PRJNA557674 | ENA

MicroRNA transcriptional profiling in serum-starved human aortic smooth muscle cells

Project description:We sought to identify microRNAs that were differentially regulated in cultured primary human aortic smooth muscle cells (SMCs) when exposed to growth arrest via serum starvation over two time points - 48 hours and 72 hours, when compared with serum-fed cells. This treatment leads to increased expression of SMC differentiation markers such as ACTA2, MYH11 and TAGLN. We identified 31 significantly regulated miRNA candidates during this process, 28 rising and 3 falling. Human aortic SMCs (AoSMCs) were propagated in growth media. Control plates were harvested, and the remaining plates were serum starved for 48 (SS48) or 72 hours (SS72) in serum-free basal media. Several arrays were excluded from final analysis after QC, resulting in a final set of 10.

2009-12-25 | E-GEOD-19544 | biostudies-arrayexpress

Single-Cell RNAseq Analysis of Murine Fate-Mapped Tsc1+/+ and Tsc1-/- Aortic Smooth Muscle Cells

Project description:Single-Cell RNAseq Analysis of Murine Fate-Mapped Tsc1+/+ and Tsc1-/- Aortic Smooth Muscle Cells

| PRJNA558136 | ENA

MicroRNA transcriptional profiling in serum-starved human aortic smooth muscle cells

2009-12-25 | GSE19544 | GEO

Expression data from mouse aortas

Project description:Aortic aneurysm is a life-threatening cardiovascular disorder due to the predisposition for dissection and rupture. Genetic studies have proved the involvement of the transforming growth factor-β (TGF-β) pathway in aortic aneurysm. Smad4 is the central mediator of canonical TGF-β signaling. However, the exact role of Smad4 confined to the smooth muscle cells (SMCs) in the pathogenesis of aortic aneurysm is largely unknown. Furthermore, whether TGF-β signaling disruption in SMCs could directly trigger aortic wall inflammation remains poorly investigated. Recently, we revealed a pivotal role of smooth muscle Smad4 signaling in maintaining aortic wall homeostasis and protecting against the development of aortic aneurysm and dissection. To evaluate the underlying mechanism by which Smad4 regulate VSMC functions and affects aneurysm formation and development, Smooth muscle specific Smad4 Knockout mice and the control littermate were sacrificed at 6 weeks old, and their aortic ateries were collected.We combined 3-5 vessels for one sample, and 2 samples for each phenotype. Subsequently, a total of 400ng RNA was used following Affymetrix instruction and 2 ug of cRNA were hybridized for 16 hr at 45°. GeneChips were scanned using the Scanner 7G and the data was analyzed with Expression Console using Affymetrix default analysis settings and global scaling as normalization method. RMA analysis was employed to evaluate the gene expression. We used microarrays to detect the global gene expression in the aortic arteries of smooth muscle cell specific Smad4 knockout mice (Smad4-KO)compared with wild type littermates (WT) at 6 weeks old and identified distinct classes of altered genes.

2016-12-01 | GSE67182 | GEO

Smooth muscle cell-specific Klf4 deletion in Marfan syndrome aortic root aneurysm

Project description:Aortic smooth muscle cell (SMC) phenotype modulation is a central feature of cell-mediated pathology in Marfan syndrome aortic aneurysm and Klf4 is proposed to contribute to this process. We generated mice with smooth muscle cell-specific Klf4 deletion using an Myh11-creERT2 transgene, induced deletion at 8 weeks and performed single cell RNA sequencing at 24 weeks on whole aortic root tissues.

2022-08-23 | GSE206227 | GEO

Cholesterol and TNF-induced transcriptomic changes in Mus musculus aortic smooth muscle cells

Project description:To map gene regulation downstream of cholesterol overload and NF-kappaB signaling in smooth muscle cells (SMCs), we cultured primary aortic SMCs from wildtype mice with cyclodextrin-complexed cholesterol or the prototypical NF-kappaB activator, tumor necrosis factor (TNF), or both.

2023-05-29 | E-MTAB-12069 | biostudies-arrayexpress

Effect of H2O2 and Collagen tripeptide (CTP) on endothelial cells and smooth muscle cells in cell culture

Project description:Analysis of gene expression in primary cultured human aortic endothelial cells (HAECs) and primary cultured human aortic smooth muscle cells (SMCs) with or without H2O2 or Collagen tripeptide (CTP)

2021-06-29 | GSE175612 | GEO

Generation and comparative analysis of an Itga8-CreERT2 mouse with preferential activity in vascular smooth muscle cells

Project description:All current smooth muscle cell (SMC) restricted Cre mice recombine floxed alleles in vascular and visceral SMCs. We generated a tamoxifen-inducible CreERT2 mouse, Itga8-CreERT2, and compared its activity to the widely used Myh11-CreERT2 mouse. Both CreERT2 mice showed similar activity in vascular SMCs; however, Itga8-CreERT2 displayed low activity in visceral SMC-containing tissues (e.g., intestine). Myh11-CreERT2 (but not Itga8-CreERT2) mice exhibited high levels of CreERT2 protein, tamoxifen-independent activity, and an altered transcriptome. Whereas Myh11-CreERT2-mediated knockout of Srf resulted in a lethal intestinal phenotype, loss of Srf with Itga8-CreERT2 (SrfItga8) revealed viable mice with attenuated vascular SMC contractile gene expression, but no evidence of intestinal pathology. Male and female SrfItga8 mice presented with vascular contractile incompetence; however, only male SrfItga8 mice showed systemic changes in blood pressure. These results establish the Itga8-CreERT2 mouse as an alternative to existing SMC Cre strains where gene loss may result in visceral myopathies that obfuscate accurate phenotyping in vascular SMCs.

2022-09-13 | GSE199244 | 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