Exocytosis regulation of [Cl^-]i and G protein in gastric mucous cells.

胃粘膜细胞中 [Cl^-]i 和 G 蛋白的胞吐作用调节。

• 批准号: 11670052
• 负责人: NAKAHARI Takashi
• 金额: $ 2.18万
• 依托单位: Osaka Medical College
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11670052/
• 关键词: exocytosis; intracellular Ca2+ concentration; gastric mucin secretion; cell volume; antral mucous cell; intracellular Cl- concentration; pertusis toxin; G protein; intracellular Cl concentration; video-microscopy; exocytosis; intracellular Ca^<

Acetylcholine (ACh, 10 μM) stimulation caused cell shrinkage and activation of exocytotic events mediated via intracellular Ca^<2+> concentration ([Ca^<2+>]i) in antral mucus cells of guinea pig, and ACh- evoked exocytosis was modulated by cell shrinkage. Application of a hyposmotic stress, infusion of Cl^--free solution and addition of bumetanide, which caused reduction of [Cl^-]i, potentiated ACh- evoked exocytotic events. These indicate that decreases in [Cl^-]i appears to potentiate ACh-evoked exocytotic events. Isolated antral mucus cells were treated with nystatin to alter [Cl^-]i. As [Cl^-li increase from 5 to 155.5 mM, the frequency of ACh-evoked exocytotic events declines approximately 50%. Thus, reduction of [Cl-]i potentiated ACh-evoked exocytotic events. Treatment with pertussis toxin (PTX), which inhibits G proteins, eliminated the [Cl^-]i dependency of ACh-evoked exocytosis. The Ca^<2+>-regulated exocytosis was modulated by G proteins, which are PTX-sensitive and inhibited by intracellular Cl^-.

乙酰胆碱(ACh，10μM)刺激可引起豚鼠胃窦粘液细胞内钙离子浓度([Ca^&lt；2+&gt；]i)介导的细胞收缩和胞吐活动的激活，细胞收缩对乙酰胆碱引起的胞吐起调节作用。施加低渗应激、注入无氯溶液和加入布美他尼使[Cl^-]i降低，可增强ACh诱发的胞吐活动。这些结果表明，[Cl^-]i的减少似乎增强了ACh诱发的胞吐事件。分离的胃窦粘液细胞用制霉菌素改变[Cl^-]i，当[Cl^-Li]从5 mM增加到155.5 mM时，ACh诱发的胞吐事件的频率下降约50%。因此，[Cl-]i的减少增强了ACh诱发的胞吐事件。用抑制G蛋白的百日咳毒素(PTX)处理，可消除ACh引起的胞吐对[Cl^-]i的依赖。钙离子调节的胞吐作用受G蛋白的调节，G蛋白对PTX敏感，并受细胞内氯离子的抑制。

项目成果

大西敦子: "プロスタグランジンE2による胃幽門腺粘液開口放出反応の調節:プロスタノイドレセプターEP1,EP4の役割"大阪医科大学雑誌. 59・2. 66-70 (2000)

大西敦子：“前列腺素E2对胃幽门腺粘液开放反应的调节：前列腺素受体EP1和EP4的作用”大阪医科大学杂志59・2（2000年）。

大西敦子: "Prostaglandin E2による胃幽門腺細胞からの粘液開口放出反応:細胞内Ca2+調節"大阪医科大学雑誌. 58・2. 83-87 (1999)

大西敦子：“前列腺素 E2 引起的胃幽门腺细胞的粘液胞吐反应：细胞内 Ca2+ 的调节”大阪医科大学杂志 58・2（1999）。

T.Nakahari, H.Yoshida, Y.Imai, S.Fujiwara, A.Ohnishi, C.Shimamoto, K.Katsu: "Inhibition of Ca2+ entry caused by depolarization in acetylcholine-stimulated antral mucous cells of guinea pig : G protein regulation of Ca2+ permeable channels."Jpn.J.Physiol..

T.Nakahari、H.Yoshida、Y.Imai、S.Fujiwara、A.Ohnishi、C.Shimamoto、K.Katsu：“乙酰胆碱刺激的豚鼠胃窦粘液细胞去极化引起的 Ca2 进入抑制：G 蛋白调节

Takashi Nakahari: "[Na+]i,[K+]i,[Cl-]i, regulation of exocytosis in guinea-pig antral mucous cells.,"Journal of Korean Medical Science. 15(supple). S36-37 (2000)

Takashi Nakahari：“[Na ]i、[K]i、[Cl-]i，豚鼠胃窦粘液细胞胞吐作用的调节”，《韩国医学杂志》。

Takashi Nakahari: "Accumulation of cAMP evoked by acetylcholine stimulation in rat submandibular acinar cells : observation of exocytosis, fluid secretion and [Ca2+]i"Experimental Physiology. 85.2. 159-169 (2000)

Takashi Nakahari：“大鼠颌下腺泡细胞中乙酰胆碱刺激引起的 cAMP 积累：胞吐作用、液体分泌和 [Ca2]i 的观察”实验生理学。