RGS3 and RGS4 are GTPase activating proteins in the heart

Shaosong Zhang, Ned Watson, Joseph Zahner, Jeffrey N. Rottman, Kendall J. Blumer, Anthony J. Muslin

Research output: Contribution to journalArticlepeer-review

54 Scopus citations


RGS family members are regulatory molecules that act as GTPase activating proteins (GAPs) for G(α) subunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the G(iα), G(oα) and G(qα) subtypes when tested in vitro and in vivo. Although the function of RGS proteins in cardiac physiology is unknown, their ability to deactivate G(α) subunits suggests that they may inhibit the action of muscarinic, α-adrenergic, endothelin, and other agonists. To evaluate the role of RGS family members in the regulation of cardiac physiology, we investigated the expression pattern of two RGS genes in normal and diseased rat heart tissue. RGS3 and RGS4 mRNAs and proteins were detected in adult myocardium. RGS3 and RGS4 gene expression was markedly enhanced in two model systems of cardiac hypertrophy: growth factor-stimulated cultured neonatal rat cardiomyocytes and pulmonary artery-banded (PAB) mice. RGS3 and RGS4 mRNA levels were reduced in failing myocardium obtained from SHHF/Mcc-fa(cp) (SHHF) rats. These findings support the hypothesis that RGS gene expression is highly regulated in myocardium and imply that RGS family members play an important role in the regulation of cardiac function.

Original languageEnglish
Pages (from-to)269-276
Number of pages8
JournalJournal of Molecular and Cellular Cardiology
Issue number2
StatePublished - Feb 1998


  • G protein
  • GTPase activating protein
  • Neonatal cardiomyocyte
  • RGS
  • Signal transduction

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