Search Results
You are looking at 1 - 1 of 1 items for
- Author: K L Thornburg x
- Refine by access: All content x
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
Search for other papers by N N Chattergoon in
Google Scholar
PubMed
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
Search for other papers by G D Giraud in
Google Scholar
PubMed
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
Search for other papers by K L Thornburg in
Google Scholar
PubMed
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.
