DIABETIC NEUROPATHY--RECEPTORS AND SIGNALING MECHANISM

糖尿病神经病——受体和信号传导机制

• 批准号: 6124872
• 负责人: LILIANA N BERTI-MATTERA
• 金额: $ 18.01万
• 依托单位: CASE WESTERN RESERVE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1992
• 资助国家: 美国
• 起止时间: 1992-09-30 至 2001-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6124872
• 关键词: G protein; Schwann cells; adenylate cyclase; adrenergic receptor; biological signal transduction; bradykinin; cyclic AMP; diabetic neuropathy; enzyme activity; glucose; immunochemistry; laboratory rat; membrane transport proteins; muscarinic receptor; neuropeptide receptor; phospholipase C; potassium; receptor coupling; sodium; sodium potassium exchanging ATPase; stimulant /agonist; tissue /cell culture

This application Aims to identify receptor-mediated signaling pathways in peripheral nerve and their role in experimental diabetic neuropathy. In prior work with cultured Schwann cells, she has shown that endothelins regulate levels of cyclic AMP, inositol phosphates, and ionized calcium. She will now characterize the expression of endothelin receptors in peripheral nerve, and study changes in their expression and affinity, and in the expression of ET-1, during experimental diabetes induced in rats by strepto-zotocin. Then she will examine the signaling pathways modulated by endothelins, including the roles of G proteins, the activities of phospholipase C, adenylyl cyclase, and sodium, potassium ATPase. Finally, she will examine the effects if incubation of immortalized Schwann cells in high glucose media on basal and endothelin-driven signaling and cell proliferation, and examine the reversibility of the effects of high glucose elicited by diminishing glucose or myo-inositol supplements.

本应用旨在识别受体介导的信号通路