Cellular Signaling and Kidney Function

细胞信号传导和肾功能

• 批准号: 7098737
• 负责人: Douglas C. Eaton
• 金额: $ 131.43万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-09-30 至 2009-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7098737
• 关键词: biological signal transduction; biological transport; kidney function; pathologic process

Despite years of research on renal cell physiology in the normal kidney, a comprehensive understanding of the factors that govern total body homeostatic balance and associated disease states is still incomplete. However, it has become quite clear that normal homeostatic balance and the abnormal responses of the body to renal pathophysiology involves significant interaction among a variety of renal processes, systemic hormones, and responses of other tissues within the body. Although some of these interactions have been known for some time, the molecular mechanisms driving others such as apoptotic and proliferative responses have only recently been investigated. This is primarily because of new tools which are now available to study these interactions. There are cellular and molecular biological methods that make it possible to identify and modify the proteins that are responsible for maintaining normal homeostatic balance and those which are responsible for pathophysiological responses within the kidney and elsewhere in the body in response to loss of renal function. The Department of Physiology and the Division of Nephrology at Emory University have a long history of research into the identification, description and characterization of cellular processes in the kidney that are related to normal physiology and pathophysiology and how renal pathophysiology can impact other tissues in the body. The objective of this Program, Cellular and Molecular Biology of Renal Disease Processes, is to reinforce the existing interactions and develop new directions between a closely knit group of investigators who will use molecular and cellular biological tools to understand aberrations in renal cellular mechanisms that can lead to disease states and the impact of these disease states on other tissues. Project l is "ENaC Assembly, Trafficking, Degradation, and Recycling" which will characterize the apparently unique cellular processing of renal sodium channel proteins. Project 2, "The Role of Pendrin in Mineralocortieoid-Indueed Hypertension" will examine regulation of a pathway for chloride movement in the CCD. Project 3, "Insulin Signaling and Muscle Protein Turnover in Acidosis", examines the mechanisms of muscle wasting associated with renal disease. The last, Project 4, "Regulation of Urea Transporters in MDCK Cells", examines the regulation of renal urea transport proteins in a new model system.

尽管在正常肾脏中研究了多年的肾细胞生理学研究，但对控制总体体内平衡和相关疾病状态的因素的全面了解仍然不完整。然而，很明显，正常的体内平衡和人体对肾脏病理生理学的异常反应涉及各种肾脏过程，全身激素和人体其他组织的反应之间的显着相互作用。尽管其中一些相互作用已知一段时间以来，但直到最近才研究了驱动其他相互作用的分子机制，例如凋亡和增殖反应。这主要是因为现在可以研究这些相互作用的新工具。有细胞和分子生物学方法使其 可以识别和修改负责维持正常稳态平衡的蛋白质以及负责肾脏和体内其他地方的病理生理反应的蛋白质，以响应肾功能的丧失。埃默里大学生理学和肾脏科学系有悠久的研究历史 与正常的生理学和病理生理学以及肾脏病理生理学如何影响体内其他组织有关。该程序的目的，肾脏疾病过程的细胞和分子生物学的目的是加强现有的相互作用，并在紧密编织的研究者之间开发新的方向，这些研究者将使用分子和细胞生物学工具来了解肾细胞机制中的畸变，这些肾脏机制可以导致疾病状态和疾病状态和 这些疾病状态对其他组织的影响。项目L是“ ENAC组装，运输，退化和回收利用”，它将表征肾脏钠通道蛋白的明显独特的细胞加工。项目2，“ Pendrin在矿体皮层指示的高血压中的作用”将检查CCD中氯化物运动途径的调节。项目3，“酸中毒中的胰岛素信号传导和肌肉蛋白更新”，检查了肌肉的机制 浪费与肾脏疾病有关。最后一个项目4，“ MDCK细胞中尿素转运蛋白的调节”，研究了新模型系统中肾尿素转运蛋白的调节。