Blockade of calcium influx through L-type calcium channels attenuates mitochondrial injury and apoptosis in hypoxic renal tubular cells

Journal of the American Society of Nephrology : JASN
Tetsuhiro TanakaToshiro Fujita

Abstract

In hypoxia, ATP depletion causes cellular Ca(2+) increase, mitochondrial injury, and apoptosis in renal tubular cells. However, the molecular basis of these observations is incompletely delineated. IRPTC, a rat renal proximal tubular cell line, was treated with antimycin A, and disturbances in cytoplasmic calcium ([Ca(2+)]c) and mitochondrial calcium ion concentration ([Ca(2+)]m), dissipation of mitochondrial membrane potential (DeltaPsi(m)), cytochrome c release, and resultant apoptosis were examined. Pharmacologic targeting of L-type Ca(2+) channels in vitro and in vivo was used to clarify the involvement of voltage-dependent Ca(2+) channels during this process. In vitro studies indicated that ATP depletion-induced apoptosis was preceded by increased [Ca(2+)]c and [Ca(2+)]m before activation of mitochondrial signaling. Antagonizing L-type Ca(2+) channels offset these findings, suggesting [Ca(2+)]c and [Ca(2+)]m involvement. Azelnidipine administration ameliorated cellular and mitochondrial Ca(2+) accumulation, mitochondrial permeability transition, cytochrome c release, caspase-9 activation, and resultant apoptosis (15.8 +/- 0.8% versus 8.9 +/- 0.7%; P < 0.01). Similar effects of azelnidipine were substantiated in an in vivo ...Continue Reading

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