Role of matrix Gla protein in parathyroid hormone inhibition of osteoblast mineralization

Rajaram Gopalakrishnan, Supaporn Suttamanatwong, Ann E. Carlson, Renny T. Franceschi

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


Parathyroid hormone (PTH) exerts biphasic effects on bone, dependent on the frequency and dose of administration. The catabolic actions of PTH on bone have been associated with continuous treatment, an increase in osteoblast-mediated resorption of bone via osteoclast activation, and inhibition of osteoblast activity and mineralization. Downregulation of differentiation markers and inhibition of mineralization by PTH have been reported in primary calvarial explants and osteoblast cell lines. Using MC3T3-E1 osteoblast-like cells, we have shown that matrix Gla protein (MGP) can be induced by PTH, and that this induction may explain the PTH-mediated inhibition of osteoblast biomineralization. MGP is a known inhibitor of mineralization, and mice deficient in Mgp show severe vascular calcification and premature bone mineralization. This review discusses the role of MGP in mineralization, comparing bone and vascular mineralization. In addition to MGP, the regulation and possible role of osteopontin, another known regulator of osteoblast mineralization, in PTH-mediated regulation of bone and vascular mineralization is discussed.

Original languageEnglish (US)
Pages (from-to)166-175
Number of pages10
JournalCells Tissues Organs
Issue number3-4
StatePublished - Apr 2006


  • Matrix Gla protein
  • Mineralization
  • Osteoblast
  • Osteopontin
  • Parathyroid hormone
  • Vascular calcification


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