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- Author: N N Chattergoon x
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Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon, USA
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The fetal heart undergoes its own growth and maturation stages all while supplying blood and nutrients to the growing fetus and its organs. Immature contractile cardiomyocytes proliferate to rapidly increase and establish cardiomyocyte endowment in the perinatal period. Maturational changes in cellular maturation, size and biochemical capabilities occur, and require, a changing hormonal environment as the fetus prepares itself for the transition to extrauterine life. Thyroid hormone has long been known to be important for neuronal development, but also for fetal size and survival. Fetal circulating 3,5,3′-triiodothyronine (T3) levels surge near term in mammals and are responsible for maturation of several organ systems, including the heart. Growth factors like insulin-like growth factor-1 stimulate proliferation of fetal cardiomyocytes, while thyroid hormone has been shown to inhibit proliferation and drive maturation of the cells. Several cell signaling pathways appear to be involved in this complicated and coordinated process. The aim of this review was to discuss the foundational studies of thyroid hormone physiology and the mechanisms responsible for its actions as we speculate on potential fetal programming effects for cardiovascular health.
Departments of Physiology and Pharmacology and
Department of Medicine (Cardiovascular Medicine), Oregon Health and Science University, L464, 3181 SW Sam Jackson Park Rd, Portland, Oregon 97239-3098, USA
Portland Veterans Affairs Medical Center, Portland, Oregon 97201, USA
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Departments of Physiology and Pharmacology and
Department of Medicine (Cardiovascular Medicine), Oregon Health and Science University, L464, 3181 SW Sam Jackson Park Rd, Portland, Oregon 97239-3098, USA
Portland Veterans Affairs Medical Center, Portland, Oregon 97201, USA
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Departments of Physiology and Pharmacology and
Department of Medicine (Cardiovascular Medicine), Oregon Health and Science University, L464, 3181 SW Sam Jackson Park Rd, Portland, Oregon 97239-3098, USA
Portland Veterans Affairs Medical Center, Portland, Oregon 97201, USA
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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.
