Receptor-mediated net breakdown of phosphatidylinositol 4,5-bisphosphate in parotid acinar cells.
Receptor-mediated net breakdown of phosphatidylinositol 4,5-bisphosphate in parotid acinar cells.
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腮腺腺泡细胞中受体介导的磷脂酰肌醇 4,5-二磷酸的净分解。
DOI：
10.1042/bj2060555
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
PutneyJr,JW
中科院分区：
文献类型：
--
作者：
Weiss,SJ;McKinney,JS;PutneyJr,JW
研究了大鼠腮腺腺泡细胞中磷脂酰肌醇4-磷酸（PtdIns 4P）和磷脂酰肌醇4，5-二磷酸[PtdIns（4，5）P2]的代谢，特别是受体活性激动剂的作用。用乙酰甲胆碱刺激胆碱能-毒蕈碱受体引起40-50%的[32 P]PtdIns（4，5）P2迅速消失，但对PtdIns 4P没有影响。作用于α-肾上腺素受体的肾上腺素和P物质也刺激PtdIns（4，5）P2的净损失。β-肾上腺素受体激动剂异丙肾上腺素和钙离子载体离子霉素未能影响标记的PtdIns（4，5）P2或PtdIns 4P。通过用过量EGTA螯合细胞外Ca 2+，并通过消除细胞Ca 2+释放的实验方案，证明了激动剂诱导的PtdIns（4，5）P2的减少独立于Ca 2+内流和Ca 2+释放。这些结果可能表明，净PtdIns（4，5）P2的击穿是腮腺腺泡细胞的刺激-反应通路中的早期事件，并可能直接参与激动剂诱导的质膜Ca 2+释放的机制。
The metabolism of phosphatidylinositol 4-phosphate (PtdIns4P) and phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] in rat parotid acinar cells was investigated, particularly with regard to the effects of receptor-active agonists. Stimulation of cholinergic-muscarinic receptors with methacholine provoked a rapid disappearance of 40-50% of [32P]PtdIns(4,5)P2, but had no effect on PtdIns4P. Adrenaline, acting on alpha-adrenoceptors, and Substance P also stimulated net loss of PtdIns(4,5)P2. The beta-adrenoceptor agonist, isoprenaline, and the Ca2+ ionophore, ionomycin, failed to affect labelled PtdIns(4,5)P2 or PtdIns4P. By chelation of extracellular Ca2+ with excess EGTA, and by an experimental protocol that eliminates cellular Ca2+ release, it was demonstrated that the agonist-induced decrease in PtdIns(4,5)P2 is independent of both Ca2+ influx and Ca2+ release. These results may suggest that net PtdIns(4,5)P2 breakdown is an early event in the stimulus-response pathway of the parotid acinar cell and could be directly involved in the mechanism of agonist-induced Ca2+ release from the plasma membrane.