ACTH is a novel regulator of bone mass

Carlos M Isales, Mone Zaidi, Harry C. Blair

Research output: Chapter in Book/Report/Conference proceedingConference contribution

44 Scopus citations

Abstract

Adrenocorticotropin (ACTH) is one of several peptide hormones derived from a larger molecule, proopiomelanocortin (POMC). ACTH is a classic endocrine hormone, processed and secreted from the pituitary to stimulate cortisol production from the fasciculata cells in the adrenal gland. However, ACTH is also produced by other cells, including macrophages, at many sites in the body. ACTH binds to a specific member of the melanocortin receptor family, the MC2R. MC2R is expressed in osteoblastic cells in vivo, as shown by in situ hybridization. MC2R expression is strongest at sites of active bone deposition, and thus ACTH response probably varies with osteoblastic activity or stage of osteoblast differentiation. In vitro ACTH stimulates proliferation of osteoblasts in a dose-dependent manner. ACTH at 10 nM increases collagen I mRNA in the osteoblastic cell line SaOs2, although at lower concentrations ACTH may oppose osteoblast differentiation. ACTH is thus, at high concentrations, anabolic for the osteoblast, and it is highly likely that the hormone has concentration-dependent effects on bone metabolism in vivo.

Original languageEnglish (US)
Title of host publicationSkeletal Biology and Medicine
PublisherBlackwell Publishing Inc.
Pages110-116
Number of pages7
ISBN (Print)9781573317856
DOIs
StatePublished - Jan 1 2010

Publication series

NameAnnals of the New York Academy of Sciences
Volume1192
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Adrenocorticotropic hormone
  • Glucocorticoids
  • Osteoblasts
  • Osteoclasts
  • POMC

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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    Isales, C. M., Zaidi, M., & Blair, H. C. (2010). ACTH is a novel regulator of bone mass. In Skeletal Biology and Medicine (pp. 110-116). (Annals of the New York Academy of Sciences; Vol. 1192). Blackwell Publishing Inc.. https://doi.org/10.1111/j.1749-6632.2009.05231.x