We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Mid-Gestation Ovine Cardiomyocytes Are Vulnerable to Mitotic Suppression by Thyroid Hormone.
- Authors
Chattergoon, Natasha N.; Louey, Samantha; Stork, Philip; Giraud, George D.; Thornburg, Kent L.
- Abstract
Circulating fetal 3,3′,5-tri-iodo-l-thyronine (T3 ) is maintained at very low levels until a dramatic prepartum surge. 3,3′,5-Tri-iodo-l-thyronine inhibits serum-stimulated proliferation in near-term ovine cardiomyocytes, but it is not known whether midgestation myocytes are also inhibited. Because early cessation of cardiomyocyte mitosis would result in an underendowed heart, we hypothesized that 0.67 gestation (100 of 145 days gestation) ovine cardiomyocytes would be insensitive to suppressive growth effects of T3 . These younger cardiomyocytes were grown with T3 in 10% serum-enriched media for 24 hours. Physiological (0.37, 0.75, and 1.5 nmol/L) concentrations of T3 dramatically suppressed mitotic activity in cardiomyocytes (P < .001). 3,3′,5-Tri-iodo-l-thyronine stimulated phosphorylation of extracellular signal-regulated kinase and AKT (also known as Protein Kinase B [PKB]) signaling pathways. Nevertheless, the protein content of the cell cycle suppressor, p21, increased 2-fold (P < .05), and promoter, cyclin D1, decreased by 50%. Contrary to our hypothesis, elevated levels of T3 powerfully inhibit proliferation of midgestation fetal cardiomyocytes. Thus, midgestation maternal hyperthyroidism might lead to an underendowed fetal myocardium.
- Subjects
PREGNANCY; HEART cells; THYROID hormones; THYRONINES; PRENATAL depression; MUSCLE cells; MITOSIS
- Publication
Reproductive Sciences, 2012, Vol 19, Issue 6, p642
- ISSN
1933-7191
- Publication type
Article
- DOI
10.1177/1933719111432860