Store-operated Ca2+ channel in renal microcirculation and glomeruli

Rong Ma, Juan Du, Sherry Sours, Min Ding

Research output: Contribution to journalShort survey

16 Scopus citations

Abstract

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 Ca 2+ 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.

Original languageEnglish
Pages (from-to)145-153
Number of pages9
JournalExperimental Biology and Medicine
Volume231
Issue number2
DOIs
Publication statusPublished - 1 Jan 2006

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Keywords

  • Ca signaling
  • Capacitative Ca entry
  • Glomerular mesangial cell
  • Renal microcirculation
  • Store-depletion
  • Store-operated Ca channel
  • Transient receptor potential

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