Calcium preconditioning inhibits mitochondrial permeability transition and apoptosis

DOI Web Site 被引用文献2件
  • Meifeng Xu
    Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0529
  • Yigang Wang
    Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0529
  • Kyoji Hirai
    Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0529
  • Ahmar Ayub
    Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0529
  • Muhammad Ashraf
    Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0529

説明

<jats:p> We tested the hypothesis whether calcium preconditioning (CPC) reduces reoxygenation injury by inhibiting mitochondrial permeability transition (MPT). Cultured myocytes were preconditioned by a brief exposure to 1.5 mM calcium (CPC) and subjected to 3 h of anoxia followed by 2 h of reoxygenation (A-R). Myocytes were also treated with 0.2 μM/l cyclosporin A (CsA), an inhibitor of MPT, before A-R. A significant increase of viable cells and reduced lactate dehydrogenase release was observed both in CPC- and CsA-treated myocytes compared with the A-R group. Cytochrome c release was predominantly observed in the cytoplasm of myocytes in the A-R group in contrast with CPC- or CsA-treated groups, where it was restricted only to mitochondria. Similarly, the cell death by apoptosis was also markedly attenuated in these groups. Electron-dense Ca<jats:sup>2+</jats:sup> deposits in mitochondria were also less frequent. Atractyloside (20 μM/l), an adenine nucleotide translocase inhibitor, caused changes similar to those in the A-R group, suggesting a role of MPT in A-R injury. Protection by inhibition of MPT by CsA and CPC suggests that MPT plays an important role in reoxygenation/reperfusion injury. The data further suggest that preconditioning inhibits MPT by inhibiting Ca<jats:sup>2+</jats:sup>accumulation by mitochondria. </jats:p>

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