The cross-talk and secretion in intracellular signaling in parotid glands

腮腺细胞内信号传导的串扰和分泌

• 批准号: 05671546
• 负责人: TOJYO Yosuke
• 金额: $ 1.28万
• 依托单位: Health Sciences University of Hokkaido, School of Dentistry
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1993
• 资助国家: 日本
• 起止时间: 1993 至 1994
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05671546/
• 关键词: Parotid gland; Intracellular signaling; Cross-talk; Pottassium release; Intracellular calcium; Protein kinase C; muscarinic receptor; Purinergic receptor; 細胞内カルシウムイオン; 細胞外ATP; アミラーゼ分泌; ホスファターゼ阻害薬; サイフリックAMP; 唾液腺; 耳下腺細胞; ホルボールエステル; スタウロスポリン

1) Treatment with the intracellular Ca^<2+> antagonist TMB-8 or the intracellular Ca^<2+> chelator BAPTA-AM strongly suppressed the carbachol (CCh)-induced K^+ release from rat parotid acini. Combined addition of ionomycin anf thapsigargin caused a rapid increas in [Ca^<2+>] and resulted in a marked release of K^+. PMA did not potenciate the CCh-induced K^+ release. The results indicate that the K^+ release is prrimarily mediated by a rapid increase in [Ca^<2+>]_1 but is not associated with activation of proteon kinase C.2) PMA attenuated the CCh-induced increase in [Ca^<2+>]_1 through inhibition of phosphoinositide hydrolysis. Activation of protein kinase C may play a role in negative-feedback control of the muscarinic pathway in rat parotid acinar cells.3) Staurosporine enhanced Ca^<2+> entry induced by depletion of intracellular Ca^<2+> stores in rat parotid acinar cells. By contrast, the phosphatase inhibitors suppressed the Ca^<2+> entry. The results suggest that phosphorylation-dephosphorylation mechanism is involeved in the regulation of the capacitative Ca^<2+> entry.4) The increase in [Ca^<2+>]_1 induced through muscarinic receptors was inhibited by external ATP.This result suggests that is a cross-talk mechanism between muscarinic receptors and purinergic ones in rat parotid acinar cells.

1)用细胞内Ca^2+拮抗剂TMB-8或细胞内Ca^2+螯合剂BAPTA-AM处理，可强烈抑制卡巴胆碱（CCh）诱导的大鼠腮腺腺泡K^+释放。离子霉素和毒胡萝卜素的联合作用使[Ca^<2+>]迅速增加，并导致K^+的显著释放。PMA不能增强CCh诱导的K^+释放。结果表明，K^+释放主要由[Ca^<2+>]_1的迅速升高介导，而与蛋白激酶C的激活无关。2）PMA通过抑制磷酸肌醇的水解而减弱了CCh引起的[Ca^<2+>]_1的升高。蛋白激酶C的激活可能在大鼠腮腺腺泡细胞毒蕈碱途径的负反馈控制中起作用。3）星形孢菌素增强大鼠腮腺腺泡细胞内Ca^<2 +>库耗竭引起的Ca^<2 +>内流。相反，磷酸酶抑制剂抑制了Ca^2+的进入。结果表明，大鼠腮腺腺泡细胞内Ca 2+的容性内流可能通过磷酸化-去磷酸化机制进行调节。4）外源性ATP可抑制毒蕈碱受体介导的[Ca 2+] 1的增加，提示这是毒蕈碱受体与嘌呤受体之间的一种相互作用机制。

项目成果

東城庸介: "Modulatory ettect of 4β-phorbol 12-myristate 13-acetate(PMA)on carbachol-induced Ca^<2+> mobilization---" Biochemical Pharmacology. 47. 2055-2061 (1994)

Yosuke Tojo：“4β-佛波醇12-肉豆蔻酸酯13-乙酸酯(PMA)对卡巴胆碱诱导的Ca^<2+>动员的调节作用---”生化药理学47。2055-2061(1994)。

東城庸介: "Carbachl-induced potassium release in rat parotid acini:comparison of the roles of cytosolic……" Japan.J.Pharmacol.63. 439-446 (1993)

Yosuke Tojo：“Carbachl 诱导的大鼠腮腺腺泡中的钾释放：胞质的作用比较......”Japan.J.Pharmacol.63 (1993)。

東城庸介: "Modulatory effect of 4 -phorbol 12-myristate 13-acetate (PMA)on carbacol-induced Ca^<2+> mobilization…" Biochemical Pharmacology. 47. 2055-2061 (1994)

Yosuke Tojo：“4-佛波醇 12-肉豆蔻酸酯 13-乙酸酯 (PMA) 对卡巴科尔诱导的 Ca^<2+> 动员的调节作用……”《生化药理学》47。2055-2061 (1994)

Yosuke Tojyo: "Carbachol-induced potassiumrelease in rat parotid acini : comparison of the roles of cytosolic Ca^<2+> and protein kinase C." Japan.J.Pharmacol. 63. 439-446 (1993)

Yosuke Tojyo：“大鼠腮腺腺泡中卡巴胆碱诱导的钾释放：胞质 Ca^2 和蛋白激酶 C 作用的比较。”

Yosuke Tojyo: "Modulatory effect of 4beta-phorbol 12-myristate 13-acetate (PMA) on carbachol-induced Ca^<2+> mobillization in rat parotid acinar cells." Biochem.Pharmacol. 47. 2055-2061 (1994)

Yosuke Tojyo：“4β-佛波醇12-肉豆蔻酸酯13-乙酸酯(PMA)对大鼠腮腺腺泡细胞中卡巴胆碱诱导的Ca^2动员的调节作用。”