Smith J B, Selak M A, Dangelmaier C, Daniel J L
Department of Pharmacology, Temple University Medical School, Philadelphia, PA 19140.
Biochem J. 1992 Dec 15;288 ( Pt 3)(Pt 3):925-9. doi: 10.1042/bj2880925.
We showed previously that direct platelet activation by collagen involves an increase in the platelet cytosolic free Ca2+ concentration ([Ca2+]i) but that this increase is not required for the adhesion of platelets to collagen. We now report that collagen-induced arachidonic acid liberation, myosin phosphorylation and 5-hydroxytryptamine secretion are dependent on increases in [Ca2+]i, as they were markedly inhibited in platelets loaded with the acetoxymethyl ester of the Ca2+ chelator BAPTA but not in cells loaded with the acetoxymethyl ester of the non-chelating diazo-3. BAPTA also partially inhibited the rate of collagen-induced phosphatidic acid (PtdA) formation but had little effect on increases in phosphorylation of pleckstrin (47 kDa protein; P47). From these results we infer that collagen-induced increases in [Ca2+]i are required for dense granule secretion and arachidonic acid liberation, but are not necessary for stimulation of the protein kinase C pathway.
我们先前表明，胶原蛋白直接激活血小板涉及血小板胞质游离钙离子浓度（[Ca2+]i）升高，但这种升高并非血小板黏附于胶原蛋白所必需。我们现在报告，胶原蛋白诱导的花生四烯酸释放、肌球蛋白磷酸化和5-羟色胺分泌依赖于[Ca2+]i升高，因为它们在加载钙离子螯合剂BAPTA乙酰氧基甲酯的血小板中受到显著抑制，而在加载非螯合性重氮-3乙酰氧基甲酯的细胞中则未受抑制。BAPTA还部分抑制了胶原蛋白诱导的磷脂酸（PtdA）形成速率，但对普列克底物蛋白（47 kDa蛋白；P47）磷酸化增加影响不大。从这些结果我们推断，胶原蛋白诱导的[Ca2+]i升高是致密颗粒分泌和花生四烯酸释放所必需的，但对于蛋白激酶C途径的激活并非必要。
