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合成抑制胰岛B细胞中胰岛素的胞吐作用，从而导致由于抑制沉积而导致Kyi D2ATPIE D2通道的闭合。 SALPC负载的大鼠腹膜肥大细胞中的光动力作用抑制了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氧可能会干扰胞胞胞菌过程。事实证明，在大鼠胰腺B细胞中，NAII D1+IE D1/CAII D12+IE D1交换器可能有助于葡萄糖诱导的胞吐机制。有人提出，刺激细胞和豚鼠lachrymal腺体的肌上皮细胞中存在不同的CAII D12+IE D1信号传导机制，可以由不同的激动剂触发。在大鼠肾上腺炎蛋白细胞中，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，而烟碱机制似乎是毒蕈碱机制的出现。胰腺腺泡细胞中氧化应激和[CAII D12+IE D1]的氧化应激抑制了Carbachol诱导的胞吐作用，信号过程也受到应力的影响。尼古丁诱导的大鼠铬蛋白细胞中尼古丁诱导的儿茶酚胺分泌的物质抑制作用是非竞争的，这表明PESSS P抑制了烟碱受体的NAII D1+IE D1通道结构域的功能。大鼠皮质的神经元死亡可能是由于[CAII D12+IE D1] II D2I D2稳态的灾难。在小鼠回肠加密细胞中，可以诱导G蛋白和ATP的激活[CAII D12+IE D1] II D2I D2，升高。所有这些结果表明，细胞内CAII D12+IE D1在各种细胞的物理和病理过程中都起着重要作用。