Rendu F, Marche P, Viret J, Daveloose D, Leterrier F, Levy-Toledano S, Caen J P
Nouv Rev Fr Hematol (1978). 1985;27(4):293-7.
The role of platelet plasma membrane in mediating cellular response to external stimuli was investigated by studying phosphatidylinositol turnover and structural physical molecular alterations. Phosphoinositide turnover was evaluated by phosphatidylinositol breakdown and phosphatidic acid (PA) synthesis. The membrane structure was investigated by measuring fatty acid chain organization, flexibility and movements using the spin label method. When platelets are stimulated by thrombin, a rapid phosphatidylinositol bisphosphate (PIP2) breakdown is observed, accompanied by an immediate PA synthesis. At the same time a membrane-bound calcium liberation within the cell is revealed by the decrease in chlortetracycline fluorescence, and the dense granule constituent serotonin is released from the cell. These events result in disorganization of the platelet membrane as estimated by the decrease in order parameter. All these thrombin-induced effects occur in the presence of EDTA, thus being independent of external calcium and aggregation. By contrast ionophore A 23187 does not induce any PIP2 breakdown nor structural disorganization and the dense granule release measured at 10 seconds is only very weak. These results were confirmed by studies on pathological platelets in which PIP2 breakdown was normal when release was normal, such as in Glanzman thrombasthenia, or did not occur when no granule release was measurable as in Gray-platelet syndrome. It is suggested that membrane-bound calcium has a structural rather than a functional role.
通过研究磷脂酰肌醇周转以及结构物理分子改变，对血小板质膜在介导细胞对外界刺激的反应中的作用进行了研究。通过磷脂酰肌醇分解和磷脂酸（PA）合成来评估磷酸肌醇周转。使用自旋标记法通过测量脂肪酸链的组织、柔韧性和运动来研究膜结构。当血小板受到凝血酶刺激时，会观察到磷脂酰肌醇二磷酸（PIP2）迅速分解，同时伴随着PA的立即合成。与此同时，通过金霉素荧光的降低揭示了细胞内膜结合钙的释放，并且致密颗粒成分5-羟色胺从细胞中释放出来。根据序参数的降低估计，这些事件导致血小板膜紊乱。所有这些凝血酶诱导的效应在存在乙二胺四乙酸（EDTA）的情况下发生，因此与细胞外钙和聚集无关。相比之下，离子载体A 23187不会诱导任何PIP2分解，也不会导致结构紊乱，并且在10秒时测得的致密颗粒释放非常微弱。对病理血小板的研究证实了这些结果，在诸如Glanzman血小板无力症中，当释放正常时PIP2分解正常，而在诸如灰色血小板综合征中，当无法测量颗粒释放时则不会发生PIP2分解。有人提出膜结合钙具有结构而非功能作用。
