Roll of cellular Signalling systems on intraocular pressure regulation mechanisms.

细胞信号系统对眼压调节机制的影响。

• 批准号: 02670788
• 负责人: MISHIMA Hiromu
• 金额: $ 1.6万
• 依托单位: Hiroshima University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1990
• 资助国家: 日本
• 起止时间: 1990 至 1991
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-02670788/
• 关键词: Adenosine 3' : 5'-cyclic monophosphate (cAMP); Protein kinase C (PKC); Inositol phospholipid turnover system; Cross-talk between cellular signalling systems; Cultured ciliary epithelia (CE); プロテインキナ-ゼ C; プロテインキナ-ゼC(PKC); イノシト-ル1、4、5ー三燐酸(IP3); 毛様体上

We studied how drugs that alter the inositol phospholopid turnover system affected the adenosine 3' : 5'-cyclic monophosphate(cAMP)system in ciliary epithelial cells to clarify a cross-talk between cAMP system and inositol phospholipid turnover system.The cAMP increases were observed in cultured chick embryo ciliary epithelial cells stimulated with isoproterenol, forskolin or NaF. The cultured cells pretreated with 2OOnM phorbol 12myristate 13-acetate(PMA), a protein kinase C(PKC)activator showed 42% inhibition of the cAMP increase induced by isoproterenol. When cultured cells incubated with 5OuM H-7, a PKC inhibitor were pretreated with 2OOnti PMA and stimulated with isoproterenol, the inhibitory effect on cAMP increase was reduced.The cultured cells pretreated with 2OOnM PMA showed 12% inhibition of the cAMP increase induced by forskolin. No inhibition of the cAMP increase was noted in the cultured cells stimulated with NaF after 2OOnM PMA pretreatment.These findings suggest that inhibition of the cAMP system is caused by the activation of PKC. -adrenergic receptor was regarded as the affected point of PKC.

我们研究了改变纤毛上皮细胞中腺苷3'：5'-循环单磷酸（CAMP）的腺苷3'：5'-循环单磷酸腺苷（CAMP）的药物如何阐明cAMP系统和肌醇磷脂的cAMP之间的增加。 NAF。用2oonm phorbol 12mristate 13-乙酸酯（PMA）预处理的培养细胞，蛋白激酶C（PKC）活化剂显示出42％的抑制作用cAMP抑制作用，由异丙肾上腺素诱导。当培养的细胞与5OUM H-7孵育时，用2oonti PMA预处理PKC抑制剂并用异丙醇刺激，抑制对CAMP的抑制作用降低。用2oonm PMA预处理的培养细胞显示，Forskolin诱导的CAMP增加了12％的抑制作用。在2oonm PMA预处理后用NAF刺激的培养细胞中，没有发现cAMP增加的抑制作用。这些发现表明，对cAMP系统的抑制是由PKC的激活引起的。 - 肾上腺素受体被认为是PKC的影响点。