Ischemia/reperfusion induce renal tubule apoptosis by inositol 1,4,5-trisphosphate receptor and L-type Ca2+ channel opening

American Journal of Nephrology
Di WuZhe Feng

Abstract

Recent studies suggest that besides the L-type calcium channel, two calcium channels on the endoplasmic reticulum (ER), the inositol 1,4,5-trisphosphate receptor (InsP3R) and ryanodine receptor (RyR), may play a role in the apoptotic process of renal tubular cells induced by ischemia/reperfusion (I/R) injury. We used antimycin A to induce cell I/R injury in vitro and found an elevation of the cytosolic calcium concentration and consequently apoptosis. Blocking either the L-type calcium channel with nicardipine or the InsP3R with TMB-8 can inhibit cytochrome c release, activate caspase 3 and decrease the apoptotic cell number. However, blocking the RyR with dantrolene had no effect. We further found that Ca(2+) influx through the L-type channel is needed for the opening of the InsP3R which activates a cascade of Ca(2+) release from the ER store. To test these blockers in vivo, in a rat renal I/R model, pretreatment with nicardipine and TMB-8, but not dantrolene, can protect renal function. Taken together, our results suggest that after I/R injury, Ca(2+) influx through the L-type calcium channel triggers the Ca(2+) release from the InsP3R and finally induces apoptosis. The InsP3R could be a new target for the treatment of renal ...Continue Reading

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Citations

Mar 20, 2015·Journal of the American Society of Nephrology : JASN·Kornélia SzebényiBalázs Sarkadi
Sep 24, 2010·Anesthesia and Analgesia·Saadet Inan, Huafeng Wei
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Mar 16, 2017·Biotechnic & Histochemistry : Official Publication of the Biological Stain Commission·M CakirF Ozyalin
Nov 28, 2020·The American Journal of Pathology·Sun-Ji ParkYing Maggie Chen

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