RESEARCH FOR TRANSMEMBRANE SIGNALING SYSTEM OF EPIDERMAL KERATINOCYTES; INTRACELLULAR FREE CALCIUM AND CELLULAR RESPONSES.

表皮角质细胞跨膜信号系统研究；

基本信息

批准号：
02670469
负责人：
KOIZUMI Hiroko
金额：
$ 1.66万
依托单位：
HOKKAIDO 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 1992
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-02670469/
关键词：
KERATINOCYTE CALCIUM PEROXIDE SUBSTANCE P PHOSPHOLIPASE C PROTEIN KINASE C ADENYLATE CYCLASE PSORIASIS Protein kinase C phospholipase C protein kinase C adenylate cyclase 細胞内遊離カルシウムリポコルチンフォドリンエピネフリン

项目摘要

Epidermal keratinocytes proliferate and differentiate to make stratum corneum. Many chemical mediators, hormones and peptides stimulate keratinocytes to induce phosphophatidylinositol metabolism, alteration of intracellular free calcium, adenylate cyclase response activation. We elucidated that bradykinin, thrombin, substance P, beta-adrenarin, adenosine, and histamine induce increase of intracellular free calcium. These effects are mediated with synthesis of inositol 1,4,5-trisphosphate or adenylate cyclase activation. The importance of calcium as a second messenger is shown. Presence of membrane skeleton proteins such as spectrin, b-fodrin, 4.1 protein like proteins were detected immunologically and the alteration of their distribution in cultured keratinocytes were observed with the change of calcium concentration of the medium. A new technique was reported to detect peroxide produced from keratinocytes using dihydrorhodamine 123.Cross-talk among transmembrane signaling systems in keratinocytes, and drugs to influence these systems should be investigated. Abnormal keratinization and acceleration of proliferation are considered to closely realt to pathogenesis of psoriasis. The alteration of membrane signaling systems in psoriasis and the action mechanisms of the drugs used in therapy of skin diseases are under investigation.

表皮角质形成细胞增殖并分化形成角质层。许多化学介质、激素和肽刺激角质形成细胞，诱导磷脂酰肌醇代谢、细胞内游离钙的改变、腺苷酸环化酶反应的激活。我们阐明缓激肽、凝血酶、P 物质、β-肾上腺素、腺苷和组胺可诱导细胞内游离钙的增加。这些作用是通过肌醇 1,4,5-三磷酸合成或腺苷酸环化酶激活介导的。显示了钙作为第二信使的重要性。免疫学检测膜骨架蛋白如血影蛋白、b-胞缝蛋白、4.1蛋白样蛋白的存在，并观察它们在培养的角质形成细胞中的分布随培养基钙浓度的变化而变化。据报道，一种新技术使用二氢罗丹明 123 检测角质形成细胞产生的过氧化物。应研究角质形成细胞跨膜信号系统之间的串扰以及影响这些系统的药物。角化异常和增殖加速被认为与银屑病的发病机制密切相关。牛皮癣中膜信号系统的改变以及用于治疗皮肤病的药物的作用机制正在研究中。