Effect of thyroid hormone on the accumulation of mRNA for skeletal and cardiac alpha-actin in hearts from normal and hypophysectomized rats

Abstract

Skeletal alpha-actin gene products are coexpressed with cardiac alpha-actins in cardiac tissue of adult humans, cows, and pigs; in prenatal rats; and during hypertrophy due either to increased hemodynamic load or the administration of alpha-adrenergic agonists. Because there is preferential synthesis of the beta-myosin heavy chain in each case, it has been suggested that the synthesis of skeletal alpha-actin in cardiac tissue is linked to that of beta-myosin heavy chain. To test this hypothesis, thyroid hormone, which causes cardiac hypertrophy with preferential synthesis of alpha-myosin heavy chain, was administered to normal and hypophysectomized rats. Animals were sacrificed from 2 to 24 hr after the injection of either 1 or 5 micrograms of hormone per 10 g of body weight. The relative amount of mRNA for skeletal and cardiac alpha-actin was measured by using the technique of primer extension. Thyroid hormone caused a rapid increase in the amount of skeletal alpha-actin mRNA relative to controls, more than 7 times in hearts from normal animals and 15 times in hearts from hypophysectomized animals. A small increase in cardiac alpha-actin mRNA also occurred. The rapid increase in transcripts for skeletal alpha-actin under conditions where the isoform of myosin heavy chain that is being synthesized is primarily alpha demonstrates independent patterns of activation of the actin and myosin heavy chain multigene families during cardiac growth in mammals.