AJP - Heart and Circulatory Physiology, Vol 270, Issue 2 638-H644, Copyright © 1996 by American Physiological Society
Regulation of SERCA 2 expression by thyroid hormone in cultured chick embryo cardiomyocytes
D. J. Fisher, S. Phillips and T. McQuinn
Lillie Frank Abercrombie Section of Pediatric Cardiology, Department of Pediatrics, Baylor College of Medicine, Houston, Texas, USA.
We investigated the role of thyroid hormone in the physiological perinatal
increase in cardiac sarcoplasmic reticulum (SR)
Ca(2+)-adenosinetriphosphatase (ATPase) expression. We isolated and
cultured the cardiomyocytes in 10(-8) M triiodothyronine (T3) for 48 h and
then measured SR Ca(2+)-ATPase mRNA and immunodetectable protein contents
as well as SR-dependent 45Ca2+ uptake rate. We also examined the effect of
T3 on expression of the same gene in monkey kidney CV-1 cells, which do not
express thyroid hormone receptors. T3 increased cardiomyocyte SR Ca2+ pump
mRNA content by 289 +/- 35%, and immunodetectable SR Ca2+ pump protein
content by 255 +/- 44%, and SR-specific 45Ca2+ uptake rate by 189 +/- 22%
(P < 0.01 for each). In contrast, T3 had no significant effect on the
total cellular RNA or protein contents in the cardiomyocyte, and there was
no effect of T3 on Ca(2+)-ATPase mRNA content in the thyroid hormone
receptor-negative CV-1 cells. These data demonstrate that T3 increases
expression of the cardiac SR Ca2+ pump, that the effect can be localized to
the cardiomyocyte, and that the effect is dependent on thyroid hormone
receptors. These data are consistent with pretranslational and possibly
transcriptional level effect of thyroid hormone on the cardiac SR Ca2+ pump
gene (SERCA 2). The gestation-associated increase in thyroid hormone may be
at least partially responsible for the previously demonstrated perinatal
increase in cardiac SR Ca2+ pump expression.
