Mid-gestation ovine cardiomyocytes are vulnerable to mitotic suppression by thyroid hormone

Natasha N. Chattergoon, Samantha Louey, Philip Stork, George D. Giraud, Kent L. Thornburg

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)642-649
Number of pages8
JournalReproductive Sciences
Issue number6
StatePublished - Jun 2012


  • cardiomyocyte proliferation
  • cyclin D1
  • fetal heart
  • p21
  • thyroid hormone

ASJC Scopus subject areas

  • Obstetrics and Gynecology


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