Cellular and molecular consequences of calcineurin Aα gene deletion

Li Sun, Ling Ling Zhu, Neeha Zaidi, Guozhe Yang, Baljit S. Moonga, Etsuko Abe, Jameel Iqbal, Solomon Epstein, Harry C. Blair, Christopher L.H. Huang, Mone Zaidi

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

Abstract

Here we briefly review our studies that have unraveled an important role for the calcium- and calmodulin-sensitive enzyme calcineurin (CN) in bone remodeling. We find that the genetic deletion of the calcineurin Aα isoform results in osteoporosis, which is recapitulated in humans following calcineurin inhibitor therapy widely used after solid organ transplantation. Mechanistically, however, while both calcineurin inhibitors cyclosporine and tacrolimus initially stimulate osteoclastic bone resorption in humans, the predominant feature in the CNAα null mouse is a profound reduction in bone formation. We speculate that the so-called "calcineurin inhibitors" may interact with molecules other than calcineurin. The clinical relevance of these observations is explored.

Original languageEnglish (US)
Title of host publicationSkeletal Biology and Medicine, Part A
Subtitle of host publicationAspects of Bone Morphogenesis and Remodeling
PublisherBlackwell Publishing Inc.
Pages216-226
Number of pages11
ISBN (Print)9781573316842
DOIs
StatePublished - Nov 2007
Externally publishedYes

Publication series

NameAnnals of the New York Academy of Sciences
Volume1116
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

ASJC Scopus subject areas

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

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