Metabolism of inositol phosphates in parotid cells: implications for the pathway of the phosphoinositide effect and for the possible messenger role of inositol trisphosphate.
Metabolism of inositol phosphates in parotid cells: implications for the pathway of the phosphoinositide effect and for the possible messenger role of inositol trisphosphate.
复制标题
腮腺细胞中肌醇磷酸的代谢：对磷酸肌醇作用途径和肌醇三磷酸可能的信使作用的影响。
DOI：
10.1016/0024-3205(84)90006-7
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发表时间：
1984
期刊：
影响因子：
6.1
通讯作者：
PutneyJr,JW
中科院分区：
文献类型：
--
作者：
Aub,DL;PutneyJr,JW
大鼠腮腺腺泡细胞被用来调查的时间过程中形成和分解的肌醇磷酸受体活性剂。在与[3H]肌醇预孵育的细胞中，在存在10 mM LiCl（其阻断肌醇磷酸的水解）的情况下，乙酰甲胆碱（10− 4 M）导致[3H]肌醇磷酸、[3H]肌醇二磷酸和[3H]肌醇三磷酸的细胞含量显著增加。随后加入阿托品（10− 4 M），导致[3H]肌醇三磷酸和[3H]肌醇二磷酸分解，积累的[3H]肌醇磷酸几乎没有变化。数据可以拟合到一个模型，其中肌醇三磷酸和肌醇二磷酸分别由磷脂酰肌醇二磷酸和磷脂酰肌醇磷酸的磷酸二酯分解形成，肌醇磷酸由肌醇二磷酸的水解而不是由磷脂酰肌醇形成。与该模型一致的发现是，[3H]肌醇三磷酸和[3H]肌醇二磷酸水平在5秒内显著增加，而[3H]肌醇磷酸的增加在60秒时几乎检测不到。这些结果表明，在腮腺的磷酸肌醇循环激活主要是由磷酸二酯分解的聚磷酸肌醇，而不是磷脂酰肌醇。此外，结果表明，肌醇三磷酸的形成可能是足够快的，它作为第二信使信号内部Ca2+释放在这个组织。
Rat parotid acinar cells were used to investigate the time course of formation and breakdown of inositol phosphates in response to receptor-active agents. In cells preincubated with [3H]inositol and in the presence of 10 mM LiCl (which blocks hydrolysis of inositol phosphate), methacholine (10−4M) caused a substantial increase in cellular content of [3H]inositol phosphate, [3H]inositol bisphosphate and [3H]inositol trisphosphate. Subsequent addition of atropine (10−4M) caused breakdown of [3H]inositol trisphosphate and [3H]inositol bisphosphate and little change in accumulated [3H]inositol phosphate. The data could be fit to a model whereby inositol trisphosphate and inositol bisphosphate are formed from phosphodiesteratic breakdown of phosphatidylinositol bisphosphate and phosphatidylinositol phosphate respectively, and inositol phosphate is formed from hydrolysis of inositol bisphosphate rather than from phosphatidylinositol. Consistent with this model was the finding that [3H]inositol trisphosphate and [3H]inositol bisphosphate levels were substantially increased in 5 sec while an increase in [3H]inositol phosphate was barely detectable at 60 sec. These results indicate that in the parotid gland the phosphoinositide cycle is activated primarily by phosphodiesteratic breakdown of the polyphosphoinositides rather than phosphatidylinositol. Also, the results show that formation of inositol trisphosphate is probably sufficiently rapid for it to act as a second messenger signalling internal Ca2+release in this tissue.