Journal article
Germline deletion of Rgs2 and/or Rgs5 in male mice does not exacerbate left ventricular remodeling induced by subchronic isoproterenol infusion
Physiological reports, v 13(1), 70178
Jan 2025
PMID: 39746869
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Sympathoexcitation is a hallmark of heart failure, with sustained beta-adrenergic receptor (beta AR)-G protein signaling activation. beta AR signaling is modulated by regulator of G protein signaling (RGS) proteins. Previously, we reported that G alpha i/o regulation by RGS2 or RGS5 is key to ventricular rhythm regulation, while the dual loss of both RGS proteins results in left ventricular (LV) dilatation and dysfunction. Here, we tested whether sustained beta AR stimulation with isoproterenol (ISO, 30 mg/kg/day, 3 days) exacerbates LV remodeling in male mice with germline deletion of Rgs2 and/or Rgs5. Rgs2 KO and Rgs2/5 dbKO mice showed LV dilatation at baseline, which was unchanged by ISO. Rgs2 or Rgs5 deletion decreased Rgs1 expression, whereas Rgs5 deletion increased Rgs4 expression. ISO induced cardiac hypertrophy and interstitial fibrosis in Rgs2/5 dbKO mice without increasing cardiomyocyte size or LV dilation but increased expression of cardiac fetal gene Nppa, alpha-actinin, and Ca2+-/calmodulin-dependent kinase II. Single Rgs2 and Rgs5 KO mice had markedly increased CD45+ cells, whereas tissue from Rgs5 KO mice showed increased CD68+ cells, as revealed by immunohistochemistry. The results together indicate that ventricular remodeling due to Rgs2 and/or Rgs5 deletion is associated with augmented myocardial immune cell presence but is not exacerbated by sustained beta AR stimulation.
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Details
- Title
- Germline deletion of Rgs2 and/or Rgs5 in male mice does not exacerbate left ventricular remodeling induced by subchronic isoproterenol infusion
- Creators
- Shelby Dahlen - University SchoolIpsita Mohanty - Drexel UniversityBo Sun - University SchoolSanjana Nallapaneni - University SchoolPatrick Osei-Owusu (Corresponding Author) - University School
- Publication Details
- Physiological reports, v 13(1), 70178
- Publisher
- Wiley
- Number of pages
- 21
- Grant note
- HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Pharmacology and Physiology
- Web of Science ID
- WOS:001388197300001
- Scopus ID
- 2-s2.0-85214088117
- Other Identifier
- 991022197333104721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Physiology