权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Studies on molecular mechanisms of exocytosis

胞吐作用的分子机制研究

基本信息

批准号：
09460134
负责人：
HABARA Yoshiaki
金额：
$ 5.31万
依托单位：
HOKKAIDO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1999
项目状态：
已结题

项目摘要

It was suggested that nitric oxide inhibits exocytosis of insulin in pancreatic B cells, by inhibiting ATP synthesis which results in prohibition of closure of KィイD2ATPィエD2 channels due to inhibition of depolarization. Photodynamic action in SALPc-loaded rat peritoneal mast cells inhibited compound 48/80-induced exocytosis of secretory granules, indicating that singlet oxygen produced by photodynamic action may interfere with exocytotic process. It was demonstrated that, in rat pancreatic B cells, NaィイD1+ィエD1/CaィイD12+ィエD1 exchanger may contribute to glucose-induced exocytotic mechanisms. It was suggested that there were different CaィイD12+ィエD1 signalling mechanisms in acinar cells and in myoepithelial cells of guinea-pig lachrymal gland, which can be triggered with different agonists. In rat adrenal chromaffin cells, cholinergic agonist-induced exocytosis correlates with the development of both intracellular signalling mechanisms and innervation, and nicotinic mechanisms seemed to precede the appearance of muscarinic mechanisms. Carbachol-induced exocytosis is inhibited by oxidative stress in pancreatic acinar cell and [CaィイD12+ィエD1], signalling process is also disturbed the stress. Inhibition by Substance P of nicotine-induced catecholamine secretion in rat chromaffin cells is noncompetitive, suggesting that substance P inhibit the function of probably NaィイD1+ィエD1 channel domain of nicotinic receptor. Neuronal death of rat cortex can be due to disturbance of [CaィイD12+ィエD1]ィイD2iィエD2 homeostasis. In mouse ileal crypt cells, activation of G-protein and ATP can induced [CaィイD12+ィエD1]ィイD2iィエD2, elevation. All these results indicate that intracellular CaィイD12+ィエD1 plays important roles in both physiological and pathological process of various cells.

有人提出，一氧化氮通过抑制 ATP 合成来抑制胰腺 B 细胞中胰岛素的胞吐作用，从而由于抑制去极化而禁止 KiiD2ATPィD2 通道的关闭。负载 SALPc 的大鼠腹膜肥大细胞中的光动力作用抑制了化合物 48/80 诱导的分泌颗粒的胞吐作用，表明光动力作用产生的单线态氧可能干扰胞吐过程。研究表明，在大鼠胰腺 B 细胞中，NaiiD1+iiD1/CaiiD12+iiD1 交换蛋白可能有助于葡萄糖诱导的胞吐机制。表明豚鼠泪腺腺泡细胞和肌上皮细胞中存在不同的CaィイD12+ィD1信号传导机制，可以通过不同的激动剂触发。在大鼠肾上腺嗜铬细胞中，胆碱能激动剂诱导的胞吐作用与细胞内信号传导机制和神经支配的发展相关，并且烟碱机制似乎先于毒蕈碱机制的出现。卡巴胆碱诱导的胞吐作用受到胰腺腺泡细胞和[CaィイD12+ィD1]氧化应激的抑制，信号传导过程也受到应激的干扰。 P物质对尼古丁诱导的大鼠嗜铬细胞中儿茶酚胺分泌的抑制是非竞争性的，这表明P物质可能抑制烟碱受体NaiiD1+iiD1通道结构域的功能。大鼠皮质神经元死亡可能是由于[CaィイD12+ィエD1]ィイD2iエD2稳态紊乱所致。在小鼠回肠隐窝细胞中，G蛋白和ATP的激活可诱导[CaィイD12+ィエD1]ィイD2iエD2升高。这些结果表明，细胞内CaィイD12+ィエD1在多种细胞的生理和病理过程中发挥着重要作用。