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MINIREVIEW

Store-Operated Ca²⁺ Channel in Renal Microcirculation and Glomeruli

Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas 76107

To whom requests for reprints should be addressed at ¹ RES-302G, 3500 Camp Bowie Boulevard, Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX, 76107. E-mail: rma{at}hsc.unt.edu

Store-operated Ca²⁺ channel (SOC) is defined as a channel that opens in response to depletion of the internal Ca²⁺ stores. During the last decade, many investigators have made a great effort to identify and characterize SOC, and to evaluate its physiologic function and pathophysiologic relevance in a variety of cell lines, primary cultures, and native tissues. To date, accumulating evidence has demonstrated that SOC is an essential Ca²⁺ entry mechanism in vascular smooth-muscle cells of renal microvasculature and glomerular mesangial cells, both of which tightly control glomerular hemodynamics and filtration. Store-operated Ca²⁺, combined with other types of Ca²⁺ entry channels, constitutes a profile of Ca²⁺ changes in response to physiologic vasoconstrictors and, thereby, regulates renal microcirculation and mesangial function. In addition, SOC is associated with altered Ca²⁺ signaling occurring in diseased kidneys, such as diabetic nephropathy. Although the gating mechanism and molecular identity of SOC are still enigmatic and may be cell-type and tissue specific, data from several independent groups suggest that protein kinase C plays an important role in SOC activation and that certain isoforms of canonical transient receptor potential (TRPC) proteins are candidates of SOC in renal microvessels and mesangial cells.

Key Words: store-operated Ca²⁺ channel • capacitative Ca²⁺ entry • store-depletion • Ca²⁺ signaling • transient receptor potential • renal microcirculation • glomerular mesangial cell

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