CELL-MATRIX INTERACTION IN BONE - TYPE-I COLLAGEN MODULATES SIGNAL-TRANSDUCTION IN OSTEOBLAST-LIKE CELLS

被引:58
作者
GREEN, J [1 ]
SCHOTLAND, S [1 ]
STAUBER, DJ [1 ]
KLEEMAN, CR [1 ]
CLEMENS, TL [1 ]
机构
[1] UNIV CALIF LOS ANGELES, CEDARS SINAI MED CTR,RES INST,SCH MED,DEPT MED, DIV ENDOCRINOL, LOS ANGELES, CA 90048 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 1995年 / 268卷 / 05期
关键词
INTRACELLULAR CALCIUM; ADENYLATE CYCLASE; PROTEIN KINASE C; OSTEOBLASTS; INTEGRINS;
D O I
10.1152/ajpcell.1995.268.5.C1090
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:C1090 / C1103
页数:14
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