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.
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