Distinct functions of Gq and G11 proteins in coupling alpha1-adrenoreceptors to Ca2+ release and Ca2+ entry in rat portal vein myocytes.
Journal of Biological Chemistry. 1997-02-01; 272(8): 5261-5268
DOI: 10.1074/jbc.272.8.5261
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1. J Biol Chem. 1997 Feb 21;272(8):5261-8.
Distinct functions of Gq and G11 proteins in coupling alpha1-adrenoreceptors to
Ca2+ release and Ca2+ entry in rat portal vein myocytes.
Macrez-Leprêtre N(1), Kalkbrenner F, Schultz G, Mironneau J.
Author information:
(1)Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, CNRS ESA
5017, Université de Bordeaux II, 146 rue Léo Saignat, 33076 Bordeaux Cedex,
France.
In this study, we identified the subunit composition of Gq and G11 proteins
coupling alpha1-adrenoreceptors to increase in cytoplasmic Ca2+ concentration
([Ca2+]i) in rat portal vein myocytes maintained in short-term primary culture.
We used intranuclear antisense oligonucleotide injection to inhibit selectively
the expression of subunits of G protein. Increases in [Ca2+]i were measured in
response to activation of alpha1-adrenoreceptors, angiotensin AT1 receptors, and
caffeine. Antisense oligonucleotides directed against the mRNAs coding for
alphaq, alpha11, beta1, beta3, gamma2, and gamma3 subunits selectively inhibited
the increase in [Ca2+]i activated by alpha1-adrenoreceptors. A corresponding
reduction of the expression of these G protein subunits was immunochemically
confirmed. In experiments performed in Ca2+-free solution only cells injected
with anti-alphaq antisense oligonucleotides displayed a reduction of the
alpha1-adrenoreceptor-induced Ca2+ release. In contrast, in Ca2+-containing
solution, injection of anti-alpha11 antisense oligonucleotides suppressed the
alpha1-adrenoreceptor-induced stimulation of the store-operated Ca2+ influx.
Agents that specifically bound Gbetagamma subunits (anti-betacom antibody and
overexpression of a beta-adrenergic receptor kinase carboxyl-terminal fragment)
had no effect on the alpha1-adrenoreceptor-induced signal transduction. Taken
together, these results suggest that alpha1-adrenoreceptors utilize two different
Galpha subunits to increase [Ca2+]i. Galphaq may activate phosphatidylinositol
4,5-bisphosphate hydrolysis and induce release of Ca2+ from intracellular stores.
Galpha11 may enhance the Ca2+-activated Ca2+ influx that replenishes
intracellular Ca2+ stores.
DOI: 10.1074/jbc.272.8.5261
PMID: 9030598 [Indexed for MEDLINE]