We have studied the influence of thyroid hormone status in vivo on expression of the genes encoding guanine nucleotide-binding regulatory protein (G protein) α-subunits G(s)α, G(i)α(2), G(i)α(3), and both the 36-kDa form (β1) and the 35-kDa form (β2) of the β-subunit in rat ventricle. The relative amounts of immunoactive G(i)α(2) and G(i)α(3) were greater in ventricular membranes from hypothyroid animals than from euthyroid animals (1.9- and 2.6-fold, respectively). A corresponding 2.3-fold increase in G(i)α(2) mRNA was observed as well as a 1.5-fold increase in G(i)α(3) mRNA. The relative amounts of immunoactive β1 and β2 polypeptides were also increased (2.8- and 1.8-fold, respectively) in the hypothyroid state and corresponded with comparable increases in the relative levels of β1 and β2 mRNAs. No difference was seen between the amounts of G(i)α(2), G(i)α(3), β1, and β2 in the euthyroid state and the hyperthyroid state. In contrast to these effects of thyroid hormone status on G(i)α and β, the steady-state amounts of G(s)α protein and mRNA were not altered by thyroid hormone status. Thyroid hormone status did not alter sensitivity of adenylyl cyclase to stimulation by sodium fluoride or guanyl-5'-yl imidodiphosphate (GppNHp), nor did it influence GppNHp-induced inhibition of forskolin-stimulated enzyme activity. These results demonstrate that thyroid hormone status in vivo can regulate expression of specific G protein subunits in rat myocardium. However, the physiological consequences of these changes remain unclear.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Biological Chemistry|
|State||Published - 1990|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology