Thyroid Hormone Increases TGF-beta1 in Cardiomyocytes Cultures Independently of Angiotensin II Type 1 and Type 2 Receptors.

TH-induced cardiac hypertrophy in vivo is accompanied by increased cardiac Transforming Growth Factor-beta1 (TGF-beta1) levels, which is mediated by Angiotensin II type 1 receptors (AT1R) and type 2 receptors (AT2R). However, the possible involvement of this factor in TH-induced cardiac hypertrophy is unknown. In this study we evaluated whether TH is able to modulate TGF-beta1 in isolated cardiac, as well as the possible contribution of AT1R and AT2R in this response. The cardiac fibroblasts treated with T(3) did not show alteration on TGF-beta1 expression. However, cardiomyocytes treated with T(3) presented an increase in TGF-beta1 expression, as well as an increase in protein synthesis. The AT1R blockade prevented the T(3)-induced cardiomyocyte hypertrophy, while the AT2R blockage attenuated this response. The T(3)-induced increase on TGF-beta1 expression in cardiomyocytes was not changed by the use of AT1R and AT2R blockers. These results indicate that Angiotensin II receptors are not implicated in T(3)-induced increase on TGF-beta expression and suggest that the trophic effects exerted by T(3) on cardiomyocytes are not dependent on the higher TGF-beta1 levels, since the AT1R and AT2R blockers were able to attenuate the T(3)-induced cardiomyocyte hypertrophy but were not able to attenuate the increase on TGF-beta1 levels promoted by T(3).