Diminished inhibition of adhesion molecule expression in prostacyclin receptor desensitized human platelets.

H Darius, K Veit, C Binz, A Fisch, J Meyer
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引用次数: 7

Abstract

Long-term exposure of platelets to prostacyclin or iloprost (100nM, 3hr) results in receptor desensitization measured as decrease in 3H-iloprost binding sites by 47 +/- 14%. Desensitized platelets respond with an increased adhesion to endothelial cells. The mechanism of increased adhesiveness was studied by measuring the expression of the adhesion molecule CD62p (p-selectin; GMP140) on washed human platelets by flowcytometry. In thrombin stimulated platelets CD62p expression was dose-dependently reduced by iloprost. In receptor desensitized platelets IC50 for iloprost inhibition of thrombin-induced CD62p expression increased from 0.48 +/- 0.10 to 2.4 +/- 0.7 nM.

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前列环素受体脱敏的人血小板中粘附分子表达抑制减弱。
血小板长期暴露于前列环素或伊洛前列素(100nM, 3hr)会导致受体脱敏,3h -伊洛前列素结合位点减少47 +/- 14%。脱敏的血小板对内皮细胞的粘附增加。通过检测粘附分子CD62p (p-选择素)的表达,研究了粘附性增强的机制;GMP140)对洗涤后的人血小板进行流式细胞术检测。在凝血酶刺激的血小板中,伊洛prost可剂量依赖性地降低CD62p的表达。在受体脱敏的血小板中,iloprost抑制凝血素诱导的CD62p表达的IC50从0.48 +/- 0.10增加到2.4 +/- 0.7 nM。
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