Mus musculus
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ABSTRACT:
PROVIDER: PRJNA386510 | ENA |
REPOSITORIES: ENA
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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
Project description:Analysis of the effects of Bmx deficiency on Angiotensin II -induced cardiac hypertrophy
| PRJNA205523 | ENA
Project description:RORasg/sg mice have small cardiomyocytes and hypocontractile hearts with increased fibrosis. Microarrays revealed broad deficits of sarcomeric RNAs and key myogenic transcription factors, suggesting that the loss of RORa leads to impaired developmental hypertrophy through transcriptional regulation. RORasg/sg mice developed exaggerated ventricular remodeling in response to Agn II infusion. We identify novel cardioprotective roles for RORa in promoting developmental and preventing pathological cardiac hypertrophy, mediated in part through regulation of the IL-6-STAT3 pathway in cardiomyocytes and cardiac fibrosis
2021-04-12 | GSE98892 | GEO
Project description:We show that Bmx-deficiency reduces angiotensin II -induced cardiac hypertrophy and pathological gene expression
2015-09-21 | GSE47420 | GEO
Project description:Hypertension-mediated left ventricular hypertrophy and cardiac fibrosis often precede heart failure. Recent studies indicate that cytoglobin (Cygb), a globin expressed in the vasculature, increases systemic blood pressure. The present work aims to determine the role of Cygb in angiotensin II (Ang II)-induced cardiac hypertrophy and fibrosis in the mouse. Methods: Males and females global Cygb knockout (Cygb−/−), and wildtype (Cygb+/+) mice were treated with Ang II (1.5 µg/kg/day) for two weeks via subcutaneous osmotic minipumps. Cardiac function was assessed through echocardiography, and hearts were analyzed for changes in hypertrophy, fibrosis, and gene expression. Functional studies were also performed in isolated cardiac fibroblasts. Results: Cygb−/− mice from both sexes showed an increase in cardiac hypertrophy over Cygb+/+ mice. Cardiac functions were also depressed in Cygb−/− males with no changes in females. Importantly, genetic deletion of Cygb did not affect systemic blood pressure in mice, at baseline or after Ang II treatment. We established that Cygb was expressed in fibroblasts and pericytes in humans and mice hearts. Finally, we found that Cygb−/− cardiac fibroblast did not upregulate the expression of genes associated with myofibroblasts following treatment with Ang II. This was reversed following expression of human cytoglobin. Conclusions: Our findings indicate that Cygb plays a protective role in the mouse heart during Ang II-induced cardiac stress. This is the first study detailing the function of Cygb in the heart as a regulator of cardiac hypertrophy. This study also reveals a role for Cygb in regulating cardiac fibroblast activation by Ang II. NEW & NOTEWORTHY: We identified cytoglobin as an important globin in cardiac pathophysiology. Genetic deletion of cytoglobin led to exacerbation of angiotensin II-mediated cardiac hypertrophy in the absence of any effect on systemic blood pressure. Cytoglobin is expressed in cardiac fibroblasts and pericytes and is required for cardiac fibroblast activation to myofibroblast. The present study reveals for the first time a role for cytoglobin in regulating angiotensin II signaling.
2026-03-10 | GSE324288 | GEO
Project description:Background: Gq-coupled G protein-coupled receptors (GPCR) mediate the actions of a variety of messengers that are key regulators of cardiovascular function. Enhanced Gaq-mediated signaling plays an important role in cardiac hypertrophy and in the transition to heart failure. We have recently described that Gaq acts as an adaptor protein that facilitates PKCz-mediated activation of ERK5 in epithelial cells. Since the ERK5 cascade is known to be involved in cardiac hypertrophy, we have investigated the potential relevance of this pathway in Gq-dependent signaling in cardiac cells. Methodology/Principal Findings: We have explored the mechanisms involved in Gq-coupled GPCR-mediated stimulation of the ERK5 pathway and its functional consequences in cardiac hypertrophy using both cultured cardiac cells and an animal model of angiotensin- dependent induction of cardiac hypertrophy in wild-type and PKCz knockout mice. We find that PKC? is required for the activation of the ERK5 pathway by Gq-coupled GPCR in cardiomyocytes and in cardiac fibroblasts. Stimulation of ERK5 by angiotensin II is blocked upon pharmacological inhibition or siRNA-mediated silencing of PKCz in primary cultures of cardiac cells and in cardiomyocytes isolated from PKCz-deficient mice. Moreover, these mice do not develop cardiac hypertrophy upon chronic challenge with angiotensin II, as assessed by morphological, biomarker, electrocardiographic and global gene expression pattern analysis. Conclusion/Significance: Our data put forward that PKC? is essential for Gq- dependent ERK5 activation in cardiac cells and indicate a key cardiac physiological role for this recently described Gaq/PKCz/MEK5 signaling axis. Littermate wild-type and PKCz -/- male mice (32 weeks of age) were subjected to continuous infusion of angiotensin II (or PBS as a control) for 14 days, a well established model for the induction of cardiac hypertrohy
2012-01-10 | E-GEOD-29145 | biostudies-arrayexpress
Project description:Pathological cardiac hypertrophy is a key predisposing factor for heart failure (HF). This study investigates the role of the E3 ubiquitin ligase Tripartite Motif-Containing 40 (TRIM40) in cardiac hypertrophy. Using TRIM40 knockout (TRIM40-/-) and cardiac-specific overexpressing mice, pathological hypertrophy was induced by angiotensin II (Ang II) infusion or transverse aortic constriction (TAC). Results demonstrated that TRIM40 expression was upregulated in hypertrophic hearts. TRIM40 deficiency attenuated cardiac hypertrophy and dysfunction, whereas its overexpression exacerbated pathological remodeling. Mechanistically, TRIM40 binds Protein Kinase N2 (PKN2) via its B-box domain, promoting K63-linked ubiquitination at cysteine 29 that enhances PKN2 phosphorylation at Ser815 and activates downstream signaling. Pharmacological inhibition of PKN2 attenuated cardiac remodeling induced by TRIM40 overexpression. These findings indicate that TRIM40 promotes cardiac hypertrophy through K63-linked ubiquitination and activation of PKN2, identifying TRIM40 as a potential therapeutic target for HF.
2025-12-21 | GSE314005 | GEO
Project description:Endogenous Muscle Atrophy F-box Regulates Pressure Overload-Induced Cardiac Hypertrophy
| PRJNA132969 | ENA
Project description:Analysis of cardiac specific AT1 transgenic mice undergoing cardiac failure, cardiac hypertrophy and wild type aged matched controls. For detailed description of the AT1 Tg mice please refer to:; Paradis P, Dali-Youcef N, Paradis FW, Thibault G, Nemer M. Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):931-6. PMID: 10639182 [PubMed - indexed for MEDLINE]
2008-06-12 | E-GEOD-2355 | biostudies-arrayexpress