Korchak H M, Vienne K, Wilkenfeld C, Roberts C, Rich A M, Weissmann G
Trans Assoc Am Physicians. 1985;98:224-32.
Activation of the neutrophil by interaction of a ligand such as f-Met-Leu-Phe with its specific receptor elicits a prompt breakdown of PIP2 and the generation of PA via diacylglycerol. There is a rapid elevation of cytosolic calcium and activation of protein kinase C. Calcium and protein kinase C act synergistically to elicit the physiological responses. Although PIP2 breakdown and PA generation are prompt responses of neutrophils to receptor occupancy by chemoattractants, these steps can be bypassed by stimuli which directly activate protein kinase C or increase cytosolic calcium. Elevation of cytosolic Ca and activation of protein kinase C did not elicit breakdown of PIP2, indicating that phosphoinositide remodeling is not caused by activation of protein kinase C or by elevation of cytosolic calcium, nor is such a breakdown or the generation of phosphatidic acid required for the subsequent responses. The evidence indicates that PIP2 breakdown is an early event in stimulus-response coupling and is correlated with receptor-initiated generation of the signal.
诸如f -甲硫氨酰-亮氨酰-苯丙氨酸等配体与其特异性受体相互作用激活中性粒细胞，会引发磷脂酰肌醇-4,5-二磷酸（PIP2）迅速分解，并通过二酰基甘油生成磷脂酸（PA）。胞质钙迅速升高，蛋白激酶C被激活。钙和蛋白激酶C协同作用引发生理反应。尽管PIP2分解和PA生成是中性粒细胞对趋化因子占据受体的快速反应，但这些步骤可被直接激活蛋白激酶C或增加胞质钙的刺激所绕过。胞质钙升高和蛋白激酶C激活并未引发PIP2分解，这表明磷酸肌醇重塑不是由蛋白激酶C激活或胞质钙升高引起的，后续反应也不需要这种分解或磷脂酸的生成。证据表明，PIP2分解是刺激-反应偶联中的早期事件，并且与受体引发的信号产生相关。
