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Related Experiment Videos

RGS4 reduces contractile dysfunction and hypertrophic gene induction in Galpha q overexpressing mice.

J H Rogers1, A Tsirka, A Kovacs

  • 1Center for Cardiovascular Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.

Journal of Molecular and Cellular Cardiology
|February 13, 2001
PubMed
Summary

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Regulator of G protein signaling 4 (RGS4) acts as a GTPase activating protein (GAP) for Galpha q in the heart. This study shows RGS4 regulates cardiac function and its expression impacts heart disease development.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • G protein signaling

Background:

  • Galpha q GTPase activity is intrinsically low, with RGS proteins activating it in the heart, but their in vivo relevance is unclear.
  • Cardiac-specific Galpha q overexpression in mice causes hypertrophy, PKC xi translocation, embryonic gene expression, and reduced contractility.
  • Previous studies showed RGS4 expression decreased hypertrophy and ANF induction under pressure overload.

Purpose of the Study:

  • To investigate the hypothesis that RGS4 functions as a Galpha q-specific GTPase activating protein (GAP) in the in vivo heart.
  • To determine if RGS4 co-expression ameliorates the cardiac phenotype induced by Galpha q overexpression.

Main Methods:

  • Generation of dual transgenic mice with cardiac-specific Galpha q and RGS4 expression (Galpha q-40xRGS4).

Related Experiment Videos

  • Assessment of cardiac function, including fractional shortening and left ventricular dimensions.
  • Measurement of PKC xi membrane translocation and cardiac gene expression (ANF, alpha-skeletal actin mRNA).

    • Main Results:

    • In dual transgenic mice at 4 weeks, cardiac function and dimensions were normalized compared to Galpha q-overexpressing mice.
    • PKC xi translocation and cardiac gene expression (ANF, alpha-skeletal actin) were also normalized.
    • However, by 9 weeks, compound transgenic mice developed depressed cardiac contractility.

    Conclusions:

    • This study establishes RGS4 as a functional Galpha q-specific GAP in the in vivo heart.
    • Regulated expression of RGS4 has significant pathophysiological consequences for cardiac function.
    • RGS4 plays a critical role in modulating Galpha q signaling pathways in the heart.