TY - JOUR
T1 - Cell-matrix interaction in bone
T2 - Type I collagen modulates signal transduction in osteoblast-like cells
AU - Green, J.
AU - Schotland, S.
AU - Stauber, D. J.
AU - Kleeman, C. R.
AU - Clemens, T. L.
PY - 1995
Y1 - 1995
N2 - 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.
AB - 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.
KW - adenylate cyclase
KW - integrins
KW - intracellular calcium
KW - osteoblasts
KW - protein kinase C
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U2 - 10.1152/ajpcell.1995.268.5.c1090
DO - 10.1152/ajpcell.1995.268.5.c1090
M3 - Article
C2 - 7762601
AN - SCOPUS:0029002165
SN - 0363-6143
VL - 268
SP - C1090-C1103
JO - American Journal of Physiology - Cell Physiology
JF - American Journal of Physiology - Cell Physiology
IS - 5 37-5
ER -