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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): Mus musculus synthetic construct

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

Project description:Heart failure is a fairly common outcome of hypertension. Recent studies have highlighted the key role of the non-hemodynamic activity of angiotensin II (Ang II) in hypertensive heart failure via inducing cardiac inflammation. Drugs that disrupt Ang II-induced cardiac inflammation may have clinical utility in the treatment of hypertensive heart failure. A naturally occurring compound, corynoline, exhibit anti-inflammatory activities in other systems. C57BL/6 mice were injected with Ang II via a micro-osmotic pump for four weeks to develop hypertensive heart failure. The mice were treated with corynoline by gavage for two weeks. RNA-sequencing analysis was performed to explore the potential mechanism of corynoline. We found that corynoline could inhibit inflammation, myocardial fibrosis, and hypertrophy to prevent heart dysfunction, without the alteration of blood pressure. RNA-sequencing analysis indicates that the PPARα pathway is involved Ang II-induced cardiac fibrosis and cardiac remodeling. Corynoline reversed Ang II-induced PPARα inhibition both in vitro and in vivo. We further found that corynoline increases the interaction between PPARα and P65 to inhibit the NF-κB pro-inflammatory pathway in H9c2 cells. Our studies show that corynoline relieves Ang II-induced hypertensive heart failure by increasing the interaction between PPARα and P65 to inhibit the NF-κB pathway.

2022-04-09 | GSE200279 | GEO

Gene expression profiling in left cardiac ventricles of C57Bl/6J and C57Bl/6N male mice treated for 48 h with angiotensin II 500 ng/kg/min.

2014-12-12 | GSE53269 | GEO

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

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.

2022-12-24 | PXD037926 | Pride

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

2022-12-24 | GSE217304 | GEO

Gene expression profiling in left cardiac ventricles of C57Bl/6J and C57Bl/6N male mice treated for 48 h with angiotensin II 500 ng/kg/min.

Project description:Analysis of angiotensin II effect on left ventricle at gene expression level. The hypothesis tested in the present study was that angiotensin II treatment may affect gene expression in left ventricle in a strain specific manner. Results provide important information about which genes respond to angiotensin II in C57Bl/6N male mice compared to their C57Bl/6J counterparts. Total RNA obtained from isolated left ventricles from C57Bl/6J and C57Bl/6N mice subjected to 48 hours of angiotensin II infusion, via osmotic mini-pumps (500ng/kg/h) implanted sub-cutaneously, compared to sham operated controls.

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

Expression data from mouse tissue Angiotensin II treated for 0, 1, 3, 7 days

Project description:Angiotensin II (Ang II) mediated signaling plays a key role in the development of hypertension associated target organ damages. However, the gene expression changes regulated by Ang II in the early stage of acute cerebral, cardiac, renal, vascular injury remain unclear. we investigated Ang II–mediated gene expression alteration associated with the development of early cerebral, cardiac, renal, vascular injury by microarray assay in a mouse model.

2017-10-19 | GSE105114 | GEO

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

2012-03-23 | GSE35627 | GEO

Analysis of the effects of Bmx deficiency on Angiotensin II -induced cardiac hypertrophy

Project description:We show that Bmx-deficiency reduces angiotensin II -induced cardiac hypertrophy and pathological gene expression Angiotensin II or NaCl were infuced for two weeks into wild-type and Bmx-deficient mice to induce cardiac hypertrophy

2013-11-30 | E-GEOD-47420 | biostudies-arrayexpress

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.

2012-03-23 | E-GEOD-35627 | biostudies-arrayexpress

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