Heptinstall S, Glenn J, Spangenberg P
Department of Medicine, University Hospital, Queen's Medical Centre, Nottingham, U.K.
Thromb Haemost. 1992 Dec 7;68(6):727-30.
We have used the DNase I inhibition assay to study changes in G-actin after platelet activation in platelet-rich plasma (PRP) induced by ADP. Because of problems associated with depolymerization of F-actin after lysis of ADP-activated platelets in the presence of plasma, G-actin was measured using a lysis buffer that contained formaldehyde to prevent any depolymerization of F-actin. Different patterns of response were seen depending on the concentration of ADP used, and these were modified by avoiding aggregation by either not stirring the sample or by adding EDTA. The results show rapid conversion of G-actin to F-actin in association with shape change, and there is a further decrease in G-actin associated with irreversible platelet aggregation. Thus evidence is presented that actin polymerization occurs in two phases after ADP stimulation.
我们使用脱氧核糖核酸酶I抑制试验来研究富血小板血浆（PRP）中由ADP诱导的血小板活化后G-肌动蛋白的变化。由于在血浆存在的情况下ADP激活的血小板裂解后F-肌动蛋白解聚存在相关问题，因此使用含有甲醛的裂解缓冲液来测量G-肌动蛋白，以防止F-肌动蛋白的任何解聚。根据所用ADP的浓度观察到不同的反应模式，并且通过不搅拌样品或添加EDTA避免聚集来对这些模式进行修改。结果显示，随着形状变化，G-肌动蛋白迅速转化为F-肌动蛋白，并且与不可逆的血小板聚集相关的G-肌动蛋白进一步减少。因此，有证据表明，ADP刺激后肌动蛋白聚合分两个阶段发生。
