ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Regulator of G protein signaling 2 is a functionally important negative regulator of angiotensin II-induced cardiac fibroblast responses.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Although myeloid-cell RGS2 knockout does not affect Ang II-induced hypertension/organ damage in mice, high RGS2 in Gitelman/Bartter syndromes-human models of endogenous Ang II signaling antagonism-is associated with hypotensive/antiremodeling effects.Physiological reports · 2026Article
- Betaine Downregulates RARRES1 to Alleviate Cartilage Fibrosis and Promote Hyaline Cartilage Repair.International journal of molecular sciences · 2026Article
- Conditional ablation of RGS2 in myeloid cells does not influence blood pressure and organ damage in angiotensin II-induced hypertension in mice.Physiological reports · 2026Article
- PUM2 knockdown regulates the expression and alternative splicing of genes associated with myocardial fibrosis in H9C2 cells.Experimental and therapeutic medicine · 2026Article
- Adeno-associated virus-based approach for genetic modification of cardiac fibroblasts in adult rat hearts.Physiological reports · 2024Article
- RGS proteins and cardiovascular Angiotensin II Signaling: Novel opportunities for therapeutic targeting.Biochemical pharmacology · 2023Review
- Cardiac RGS Proteins in Human Heart Failure and Atrial Fibrillation: Focus on RGS4.International journal of molecular sciences · 2023Review
- Human umbilical cord mesenchymal stem cells combined with pirfenidone upregulates the expression of RGS2 in the pulmonary fibrosis in mice.Respiratory research · 2022Article
- Gitelman's and Bartter's Syndromes: From Genetics to the Molecular Basis of Hypertension and More.Kidney & blood pressure research · 2022Review
- Cardioprotective effects of early intervention with sacubitril/valsartan on pressure overloaded rat hearts.Scientific reports · 2021Article
- α7 Nicotinic acetylcholine receptor mediates right ventricular fibrosis and diastolic dysfunction in pulmonary hypertension.JCI insight · 2021Article
- The association between RGS4 and choline in cardiac fibrosis.Cell communication and signaling : CCS · 2021Article
- RgsA Attenuates the PKA Signaling, Stress Response, and Virulence in the Human Opportunistic PathogenInternational journal of molecular sciences · 2019Article
- RgsD negatively controls development, toxigenesis, stress response, and virulence in Aspergillus fumigatus.Scientific reports · 2019Article
- MicroRNA-1-Mediated Inhibition of Cardiac Fibroblast Proliferation Through Targeting Cyclin D2 and CDK6.Frontiers in cardiovascular medicine · 2019Article
- Article
- Critical effects of long non-coding RNA on fibrosis diseases.Experimental & molecular medicine · 2018Review
- GAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Effect of α7 nicotinic acetylcholine receptor activation on cardiac fibroblasts: a mechanism underlying RV fibrosis associated with cigarette smoke exposure.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Characteristics of a Regulator of G-Protein Signaling (RGS)Frontiers in microbiology · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac fibroblasts play a key role in fibrosis development in response to stress and injury. Angiotensin II (ANG II) is a major profibrotic activator whose downstream effects (such as phospholipase Cβ activation, cell proliferation, and extracellular matrix secretion) are mainly mediated via G(q)-coupled AT(1) receptors. Regulators of G protein signaling (RGS), which accelerate termination of G protein signaling, are expressed in the myocardium. Among them, RGS2 has emerged as an important player in modulating G(q)-mediated hypertrophic remodeling in cardiac myocytes. To date, no information is available on RGS in cardiac fibroblasts. We tested the hypothesis that RGS2 is an important regulator of ANG II-induced signaling and function in ventricular fibroblasts. Using an in vitro model of fibroblast activation, we have demonstrated expression of several RGS isoforms, among which only RGS2 was transiently upregulated after short-term ANG II stimulation. Similar results were obtained in fibroblasts isolated from rat hearts after in vivo ANG II infusion via minipumps for 1 day. In contrast, prolonged ANG II stimulation (3-14 days) markedly downregulated RGS2 in vivo. To delineate the functional effects of RGS expression changes, we used gain- and loss-of-function approaches. Adenovirally infected RGS2 had a negative regulatory effect on ANG II-induced phospholipase Cβ activity, cell proliferation, and total collagen production, whereas RNA interference of endogenous RGS2 had opposite effects, despite the presence of several other RGS. Together, these data suggest that RGS2 is a functionally important negative regulator of ANG II-induced cardiac fibroblast responses that may play a role in ANG II-induced fibrosis development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.