Billah M M, Lapetina E G
J Biol Chem. 1982 Nov 10;257(21):12705-8.
The addition of thrombin to horse platelets prelabeled with 32P induces a rapid decrease of the radioactivity from phosphatidylinositol 4,5-bisphosphate. Maximum loss of the radioactivity from phosphatidylinositol 4,5-bisphosphate occurs with 10 s of stimulation and is followed by an increased incorporation of 32P into this lipid. The stimulation of phosphatidylinositol 4,5-bisphosphate loss by thrombin is concentration-dependent. The ionophore A23187, which mobilizes Ca2+, is ineffective in inducing the degradation of phosphatidylinositol 4,5-bisphosphate. Measurements of polyphosphoinositides by phosphorus estimation show that, 10 s after thrombin stimulation, there is a decrease of 15-20% of the total phosphatidylinositol 4,5-bisphosphate without any significant change in phosphatidylinositol 4-monophosphate. It appears that thrombin causes a rapid and transient degradation of phosphatidylinositol 4,5-bisphosphate and that this effect might be related to the initiation of platelet activation.
向预先用³²P标记的马血小板中添加凝血酶,会导致磷脂酰肌醇4,5 - 二磷酸的放射性迅速降低。磷脂酰肌醇4,5 - 二磷酸的放射性在刺激10秒时出现最大程度的损失,随后³²P掺入该脂质的量增加。凝血酶对磷脂酰肌醇4,5 - 二磷酸损失的刺激呈浓度依赖性。可动员Ca²⁺的离子载体A23187在诱导磷脂酰肌醇4,5 - 二磷酸降解方面无效。通过磷测定法对多磷酸肌醇的测量表明,在凝血酶刺激10秒后,总磷脂酰肌醇4,5 - 二磷酸减少了15 - 20%,而磷脂酰肌醇4 - 单磷酸没有任何显著变化。看来凝血酶会导致磷脂酰肌醇4,5 - 二磷酸迅速且短暂的降解,并且这种效应可能与血小板活化的起始有关。