Cell-matrix interaction in bone: Type I collagen modulates signal transduction in osteoblast-like cells

J. Green, S. Schotland, D. J. Stauber, C. R. Kleeman, T. L. Clemens

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


Cell interaction with extracellular matrix (ECM) modulates cell growth and differentiation. By using in vitro culture systems, we tested the effect of type I collagen (Coll-I) on signal transduction mechanisms in the osteosarcoma cell line UMR-106 and in primary cultures from neonatal rat calvariae. Cells were cultured for 72 h on Coll-I gel matrix and compared with control cells plated on plastic surfaces. Agonist-dependent and voltage- dependent rises in cytosolic Ca2+ concentration ([Ca2+](i); measured by fura 2 fluorometry) were significantly blunted in cells cultured on Coll-I compared with cells grown on plastic. In UMR-106 cells, the collagen matrix effect was mimicked by 24-h incubation with soluble Coll-I or short peptides containing the arginine-glycine-aspartate motif. Accumulation of cellular adenosine 3',5'-cyclic monophosphate (cAMP) stimulated by parathyroid hormone, cholera toxin, and forskolin was augmented (50-150%) in cells plated on Coll-I vs. control. The collagen effect on both [Ca2+](i)- and adenylate cyclase-signaling pathways in UMR-106 cells was abrogated in the presence of protein kinase C (PKC) depletion or inhibition. Also, Coll-I induced a twofold increase in membrane-bound PKC without changing cytosolic PKC activity. Thus, by altering PKC activity, Coll-I modulates the [Ca2+](i)- and cAMP-signaling pathways in osteoblasts. This, in turn, may influence bone remodeling processes.

Original languageEnglish (US)
Pages (from-to)C1090-C1103
JournalAmerican Journal of Physiology - Cell Physiology
Issue number5 37-5
StatePublished - 1995
Externally publishedYes


  • adenylate cyclase
  • integrins
  • intracellular calcium
  • osteoblasts
  • protein kinase C

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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