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肌醇1,4,5-三磷酸受体的激动剂依赖性磷酸化:胰腺腺泡细胞中激动剂特异性钙振荡的一种可能机制。

Agonist-dependent phosphorylation of the inositol 1,4,5-trisphosphate receptor: A possible mechanism for agonist-specific calcium oscillations in pancreatic acinar cells.

作者信息

LeBeau A P, Yule D I, Groblewski G E, Sneyd J

机构信息

Mathematical Research Branch, National Institutes of Health, Bethesda, Maryland, USA.

出版信息

J Gen Physiol. 1999 Jun;113(6):851-72. doi: 10.1085/jgp.113.6.851.

Abstract

The properties of inositol 1,4,5-trisphosphate (IP3)-dependent intracellular calcium oscillations in pancreatic acinar cells depend crucially on the agonist used to stimulate them. Acetylcholine or carbachol (CCh) cause high-frequency (10-12-s period) calcium oscillations that are superimposed on a raised baseline, while cholecystokinin (CCK) causes long-period (>100-s period) baseline spiking. We show that physiological concentrations of CCK induce rapid phosphorylation of the IP3 receptor, which is not true of physiological concentrations of CCh. Based on this and other experimental data, we construct a mathematical model of agonist-specific intracellular calcium oscillations in pancreatic acinar cells. Model simulations agree with previous experimental work on the rates of activation and inactivation of the IP3 receptor by calcium (DuFour, J.-F., I.M. Arias, and T.J. Turner. 1997. J. Biol. Chem. 272:2675-2681), and reproduce both short-period, raised baseline oscillations, and long-period baseline spiking. The steady state open probability curve of the model IP3 receptor is an increasing function of calcium concentration, as found for type-III IP3 receptors by Hagar et al. (Hagar, R.E., A.D. Burgstahler, M.H. Nathanson, and B.E. Ehrlich. 1998. Nature. 396:81-84). We use the model to predict the effect of the removal of external calcium, and this prediction is confirmed experimentally. We also predict that, for type-III IP3 receptors, the steady state open probability curve will shift to lower calcium concentrations as the background IP3 concentration increases. We conclude that the differences between CCh- and CCK-induced calcium oscillations in pancreatic acinar cells can be explained by two principal mechanisms: (a) CCK causes more phosphorylation of the IP3 receptor than does CCh, and the phosphorylated receptor cannot pass calcium current; and (b) the rate of calcium ATPase pumping and the rate of calcium influx from the outside the cell are greater in the presence of CCh than in the presence of CCK.

摘要

胰腺腺泡细胞中依赖肌醇1,4,5 -三磷酸(IP3)的细胞内钙振荡特性,关键取决于用于刺激它们的激动剂。乙酰胆碱或卡巴胆碱(CCh)会引起高频(周期为10 - 12秒)的钙振荡,且叠加在升高的基线之上,而胆囊收缩素(CCK)则会引起长周期(周期>100秒)的基线尖峰。我们发现,生理浓度的CCK会诱导IP3受体快速磷酸化,而生理浓度的CCh则不会。基于此及其他实验数据,我们构建了胰腺腺泡细胞中激动剂特异性细胞内钙振荡的数学模型。模型模拟结果与先前关于钙对IP3受体激活和失活速率的实验工作(DuFour, J.-F., I.M. Arias, and T.J. Turner. 1997. J. Biol. Chem. 272:2675 - 2681)相符,并重现了短周期、升高基线的振荡以及长周期基线尖峰。模型IP3受体的稳态开放概率曲线是钙浓度的递增函数,正如Hagar等人(Hagar, R.E., A.D. Burgstahler, M.H. Nathanson, and B.E. Ehrlich. 1998. Nature. 396:81 - 84)对III型IP3受体所发现的那样。我们使用该模型预测去除细胞外钙的影响,这一预测得到了实验证实。我们还预测,对于III型IP3受体,随着背景IP3浓度增加,稳态开放概率曲线将向较低钙浓度偏移。我们得出结论,胰腺腺泡细胞中CCh和CCK诱导的钙振荡差异可由两个主要机制解释:(a)CCK比CCh导致更多的IP3受体磷酸化,且磷酸化的受体不能通过钙电流;(b)存在CCh时钙ATP酶泵浦速率和细胞外钙内流速率比存在CCK时更大。

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