Insulin-like growth factor I production is essential for anabolic effects of thyroid hormone in osteoblasts

Bill K. Huang, Laurence A. Golden, Gabor Tarjan, Laird D. Madison, Paula H Stern*

*Corresponding author for this work

Research output: Contribution to journalArticle

61 Scopus citations

Abstract

Thyroid hormone (T3) and insulin-like growth factor I (IGF-I) are critical regulators of skeletal function. T3 increases IGF-I production in bone. To assess the potential role of IGF-I as a mediator of T3 actions, we characterized phenotypic markers of osteoblast activity in two osteoblast models, normal mouse osteoblasts and MC3T3-E1 cells, exposed to T3 alone or under conditions that interfere with IGF-I actions. T3 significantly increased osteoblast 3H-proline incorporation, alkaline phosphatase (ALP), and osteocalcin. Both αIR3, a neutralizing monoclonal antibody to the IGF-I receptor, and JB1, an IGF-I analogue antagonist, attenuated the stimulatory effects of T3. T3 effects also were decreased in cells transfected with antisense oligonucleotide (AS-ODN) to the IGF-I receptor gene. Both IGF-I and T3 had mitogenic effects that were inhibited by the antagonists. IGF-I by itself did not stimulate 3H-proline incorporation, ALP, and osteocalcin in the models used, revealing that although IGF-I is essential for the anabolic effects of T3, it acts in concert with other factors to elicit these phenotypic responses.

Original languageEnglish (US)
Pages (from-to)188-197
Number of pages10
JournalJournal of Bone and Mineral Research
Volume15
Issue number2
StatePublished - Feb 24 2000

Keywords

  • Bone formation markers
  • Growth factor regulation
  • Insulin-like growth factor I
  • Osteoblasts
  • Thyroid hormone

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Orthopedics and Sports Medicine

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