van Marwijk Kooy M, Akkerman J W, van Asbeck S, Borghuis L, van Prooijen H C
Department of Haematology, University Hospital Utrecht, The Netherlands.
Br J Haematol. 1993 Feb;83(2):253-8. doi: 10.1111/j.1365-2141.1993.tb08280.x.
Previous studies have shown that ultraviolet B (UVB) radiation causes platelet aggregation by exposing fibrinogen binding sites via activation of an intracellular mechanism. In the present study we have further investigated the routes of platelet activation following UVB exposure. Evidence is provided that UVB radiation does not activate the platelets via the classical Phospholipase A2 and Phospholipase C routes. Despite this observation, UVB-induced fibrinogen binding was found to be correlated with a 40% increase in phosphorylated 47 kD protein. Both findings could be completely inhibited in the presence of staurosporine, a potent inhibitor of protein kinase C (PK-C). In efforts to explain the mechanism of PK-C activation by UV radiation we found that both UV-induced PK-C activation and platelet aggregation were significantly reduced in the presence of specific scavengers for reactive oxygen species including superoxide dismutase and catalase. We conclude that exposure of platelets to UVB radiation can activate PK-C via oxygen radicals, resulting in exposure of fibrinogen binding sites and subsequent platelet aggregation.
先前的研究表明，紫外线B（UVB）辐射通过激活细胞内机制使纤维蛋白原结合位点暴露，从而导致血小板聚集。在本研究中，我们进一步探究了UVB照射后血小板激活的途径。有证据表明，UVB辐射不会通过经典的磷脂酶A2和磷脂酶C途径激活血小板。尽管有此观察结果，但发现UVB诱导的纤维蛋白原结合与磷酸化47 kD蛋白增加40%相关。在蛋白激酶C（PK-C）的强效抑制剂星形孢菌素存在的情况下，这两个发现均可被完全抑制。为了解释UV辐射激活PK-C的机制，我们发现，在存在包括超氧化物歧化酶和过氧化氢酶在内的活性氧特异性清除剂的情况下，UV诱导的PK-C激活和血小板聚集均显著降低。我们得出结论，血小板暴露于UVB辐射可通过氧自由基激活PK-C，导致纤维蛋白原结合位点暴露及随后的血小板聚集。
