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MiRNAs expression profiling from mouse heart after Ang II (angiotensin II) (1500ng/kg/min) infusion for 3 days and 7 days

ABSTRACT: Angiotensin II stimulates fibroblast proliferation and substantially alters gene expression patterns leading to cardiac remodeling, but the mechanisms for such differences are unknown. MicroRNAs are a novel mechanism for gene expression regulation. Herein we tested the miRNAs patterns in mouse heart using microarray assay, and investigated their role in angiotensin II-induced cardiac remodeling.

ORGANISM(S): synthetic construct Mus musculus

PROVIDER: GSE69559 | GEO | 2015/06/05

SECONDARY ACCESSION(S): PRJNA285853

REPOSITORIES: GEO

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miRNAs expression profiling from mouse heart after Ang II (angiotensin II) (1500ng/kg/min) infusion for 3 days and 7 days

Project description:Angiotensin II stimulates fibroblast proliferation and substantially alters gene expression patterns leading to cardiac remodeling, but the mechanisms for such differences are unknown. MicroRNAs are a novel mechanism for gene expression regulation. Herein we tested the miRNAs patterns in mouse heart using microarray assay, and investigated their role in angiotensin II-induced cardiac remodeling. In this study, nine samples (three groups) from mouse were used to acquire the miRNA expression profiling and the function of the abudant miRNAs in the heart were analyzed by bioinformatic methods.

2015-06-05 | E-GEOD-69559 | biostudies-arrayexpress

Corynoline protects Ang II-induced hypertensive heart failure by increasing PPARα and inhibiting NF-κB pathway

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Project description:Understanding the molecular mechanisms of pathological vascular remodeling is important for treating cardiovascular diseases and complications. Recent studies have highlighted a role of deubiquitinases in vascular pathophysiology. In this study, we investigated the role of a deubiquitinase, OTUD1, in angiotensin II (Ang II)-induced vascular remodeling. We identified upregulated OTUD1 in the vascular endothelium of Ang II-challenged mice and showed OTUD1 deletion attenuated vascular remodeling, collagen deposition, and EndMT. Conversely, OTUD1 overexpression aggravated these pathological changes both in vivo and in vitro. Mechanistically, SMAD3 was identified as a substrate of OTUD1 using co-immunoprecipitation followed with LC-MS/MS. We found OTUD1 stabilizes SMAD3 and facilitates SMAD3/SMAD4 complex formation and subsequent nuclear translocation through both K48- and K63-linked deubiquitination. OTUD1-mediated SMAD3 activation regulate the transcription of genes involved in vascular EndMT and remodeling in HUVECs. Finally, SMAD3 inhibition reversed OTUD1-promoted vascular remodeling. Our findings demonstrate endothelial OTUD1 promoted Ang II-induced vascular remodeling by deubiquitinating SMAD3. This study identified SMAD3 as a target of OTUD1 and indicates OTUD1 as a potential therapeutic target for the diseases related to vascular remodeling.

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Endothelial OTUD1 promotes Ang II-induced vascular remodeling by deubiquitinating SMAD3

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2014-12-12 | E-GEOD-53269 | biostudies-arrayexpress

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Expression data from Angiotensin II (Ang II)-treated Rat Vascular Smooth Muscle Cells (RVSMC)

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Expression data from Angiotensin II (Ang II)-treated Rat Vascular Smooth Muscle Cells (RVSMC)

Project description:Angiotensin II (Ang II)-mediated vascular smooth muscle cells (VSMC) dysfunction plays a critical role in cardiovascular diseases. However, the gene expression in this process is unclear. We used Rat Affymetrix gene array to profile Ang II-regulated gene in RVSMC and evaluated their role in VSMC dysfunction. Examined 4 samples of Rat VSMC in triplicate. Control (without Ang II treatment) and 3 samples treated with Ang II for 6h, 12h, and 24h. Compared the changes in gene expression in Ang II treated samples relative to control samples.

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