Collagen type IV stimulates an increase in intracellular Ca2+ in pancreatic acinar cells via activation of phospholipase C.

摘要: Intracellular Ca2+ responses to extracellular matrix molecules were studied in suspensions of pancreatic acinar cells loaded with Fura-2. Collagen type I, laminin, fibrinogen and fibronectin unable raise cytosolic free concentration ([Ca2+]i), whereas collagen IV, at concentrations from 5 50 micrograms/ml, significantly increased it. The effect IV was not due possible contamination type-I transforming growth factor beta or plasminogen, as neither these agents able increase [Ca2+]i. Using highly specific mass assays, inositol lipids, 1,2-diacylglycerol (DAG) Ins(1,4,5) P3 measured stimulated IV. A decrease the PtdIns(4,5) P2 PtdIns4 P a concomitant DAG InsP3 observed, showing that increases [Ca2+]i by activation phospholipase C. observed signals had two components, first resulting release intracellular stores, second flux medium through verapamil-insensitive channels. tyrosine kinase inhibitor (tyrphostine) block lipid signalling caused which together insensitivity this pathway cholera toxin pertussis preactivation protein C, longer duration lag period needed for observation than carbachol (50 mM) suggest C is activation. Inositol also Arg-Gly-Asp (RGD)-containing peptide but Arg-Asp-Gly (RDG)-containing peptide. RGD-containing peptide, carbachol, competed increasing concentration, suggesting binding site responsible contains RGD sequence. Together present results that, cells, sequence(s) within cause kinase, probably one integrin receptors, then stimulates