TGF-β1 calcium signaling in osteoblasts

Leon J. Nesti, E. J. Caterson, Wan Ju Li, Richard Chang, Thane D. McCann, Jan B. Hoek, Rocky S. Tuan*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

41 Scopus citations


Transforming growth factor-β1 (TGF-β1) action is known to be initiated by its binding to multiple cell surface receptors containing serine/threonine kinase domains that act to stimulate a cascade of signaling events in a variety of cell types. We have previously shown that TGF-β1 and BMP-2 treatment of primary human osteoblasts (HOBs) enhances cell-substrate adhesion. In this report, we demonstrate that TGF-β1 elicits a rapid, transient, and oscillatory rise in the intracellular Ca2+ concentration, [Ca2+]i, that is necessary for enhancement of cell adhesion in HOBs but does not alter the phosphorylation state of Smad proteins. This rise in [Ca2+]i in HOB is not observed in the absence of extracellular calcium or when the cells are treated with the L-type Ca2+ channel blocker, nifedipine, but is stimulated upon treatment with the L-type Ca2+ channel agonist, Bay K 8644, or under high K+ conditions. The rise in [Ca2+]i is severely attenuated after treatment of the cells with thapsigargin, a selective endoplasmic reticulum Ca2+ pump inhibitor. TGF-β1 enhancement of HOB adhesion to tissue culture polystyrene is also inhibited in cells treated with nifedipine. These data suggest that intracellular Ca2+ signaling is an important second messenger of the TGF-β1 signal transduction pathway in osteoblast function.

Original languageEnglish
Pages (from-to)348-359
Number of pages12
JournalJournal of Cellular Biochemistry
Issue number2
StatePublished - 15 May 2007
Externally publishedYes


  • Ca channel
  • Ca signaling
  • Cell adhesion
  • Fura-2
  • Osteoblast
  • Smad
  • TGF-β1


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