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¹ Heart Research Center,
² Departments of Physiology and Pharmacology and
³ Department of Medicine (Cardiovascular Medicine), Oregon Health and Science University, L464, 3181 SW Sam Jackson Park Rd, Portland, Oregon 97239-3098, USA
⁴ Portland Veterans Affairs Medical Center, Portland, Oregon 97201, USA

(Requests for offprints should be addressed to N N Chattergoon; Email: chatterg{at}ohsu.edu)

Thyroid hormone (T₃) is a key regulator of fetal organ maturation. Premature elevations of thyroid hormone may lead to a ‘mature’ cardio-phenotype. Thyroid hormone will stimulate maturation of ovine fetal cardiomyocytes in culture by decreasing their proliferative capacity. Group 1 fetal cardiomyocytes (~135 days gestation) were incubated with T₃ (1.5, 3, 10, and 100 nM) and bromodeoxyuridine (BrdU; 10 µM) for 24 and 48 h. Group 2 cardiomyocytes were cultured with T₃ alone for later protein analysis of cell cycle regulators. At all concentrations, T₃ decreased BrdU uptake fourfold in serum media (P<0.001 versus serum, n = 5). Following serum-free (SF) T₃ treatment, BrdU uptake was inhibited when compared with serum (P<0.001 versus serum, n = 5). p21 expression increased threefold (P<0.05 versus serum free, n = 4) and cyclin D1 expression decreased twofold (P<0.05 versus serum, n = 4) in T₃-treated cardiomyocytes. (1) T₃ inhibits fetal cardiomyocyte proliferation, while (2) p21 protein levels increase, and (3) cyclin D1 levels decrease. Thus, T₃ may be a potent regulator of cardiomyocyte proliferation and maturation in the late gestation fetus.