αB-晶状体蛋白，一种低分子量热休克蛋白，充当血小板功能的调节剂。
AlphaB-crystallin, a low-molecular-weight heat shock protein, acts as a regulator of platelet function.
作者信息
Kozawa O, Matsuno H, Niwa M, Hatakeyama D, Kato K, Uematsu T
机构信息
Department of Pharmacology, Gifu University School of Medicine, Japan.
出版信息
Cell Stress Chaperones. 2001 Jan;6(1):21-8. doi: 10.1379/1466-1268(2001)006<0021:bcalmw>2.0.co;2.
It has recently been reported that alphaB-crystallin, a low-molecular-weight heat shock protein, may be released from cells by mechanical stretch. We investigated a physiological role of alphaB-crystallin in platelet function. AlphaB-crystallin inhibited platelet aggregation induced by thrombin or botrocetin in hamsters and humans. These platelets had specific binding sites for alphaB-crystallin. Moreover, alphaB-crystallin significantly reduced thrombin-induced Ca2+ influx and phosphoinositide hydrolysis by phospholipase C in human platelets. Additionally, plasma levels of alphaB-crystallin were markedly elevated in cardiomyopathic hamsters. Levels of alphaB-crystallin in vessel walls after endothelial injury were markedly reduced. Therefore, our results suggest that alphaB-crystallin, which is discharged from vessel walls in response to endothelial injury, acts intercellularly as a regulator of platelet function.
最近有报道称，αB-晶状体蛋白，一种低分子量热休克蛋白，可能会因机械拉伸而从细胞中释放出来。我们研究了αB-晶状体蛋白在血小板功能中的生理作用。αB-晶状体蛋白抑制了仓鼠和人类中由凝血酶或蛇毒凝血酶诱导的血小板聚集。这些血小板具有αB-晶状体蛋白的特异性结合位点。此外，αB-晶状体蛋白显著减少了人血小板中凝血酶诱导的Ca2+内流和磷脂酶C介导的磷酸肌醇水解。另外，心肌病仓鼠血浆中αB-晶状体蛋白水平显著升高。内皮损伤后血管壁中αB-晶状体蛋白水平显著降低。因此，我们的结果表明，响应内皮损伤而从血管壁释放的αB-晶状体蛋白在细胞间作为血小板功能的调节剂发挥作用。
Zotero 插件