Oxygen Glucose Deprivation (OGD)/Re-Oxygenation-Induced In Vitro Neuronal Cell Death Involves Mitochondrial Cyclophilin-D/P53 Signaling Axis. | |
MedLine Citation:
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PMID: 23322110 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Oxidative stress-induced neuronal cell death requires opening of the mitochondrial permeability transition pore. P53 mitochondrial translocation and association with Cyclophilin D (Cyp-D) is required for the pore opening. Here we tested this signaling axis in oxygen glucose deprivation (OGD)/re-oxygenation-induced in vitro neuronal death. Using mitochondrion immunoprecipitation, we found that p53 translocated to mitochondrion and associated with Cyp-D in SH-SY5Y cells exposed to (OGD)/re-oxygenation. Disruption of this complex by Cyp-D inhibitor Cyclosporine A (CsA), or by Cyp-D or p53 deficiency, significantly inhibited OGD/re-oxygenation-induced apoptosis-independent cell death. Conversely, over-expression of Cyp-D in SH-SY5Y cells caused spontaneous cell death, and these cells were more vulnerable to OGD/re-oxygenation. Finally, CsA or Cyp-D RNAi suppressed OGD/re-oxygenation-induced neuronal cell death in primary cultures. Together, our study suggests that OGD/re-oxygenation-induced in vitro cell death involves a mitochondrial Cyp-D/p53 signaling axis. |
Authors:
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Li-Ping Zhao; Chao Ji; Pei-Hua Lu; Chen Li; Bo Xu; Hong Gao |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2013-1-16 |
Journal Detail:
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Title: Neurochemical research Volume: - ISSN: 1573-6903 ISO Abbreviation: Neurochem. Res. Publication Date: 2013 Jan |
Date Detail:
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Created Date: 2013-1-16 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7613461 Medline TA: Neurochem Res Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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State Key Laboratory of Reproductive Medicine, Department of Anesthesiology, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, 140 Hanzhong Road, Nanjing, 210029, China. |
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MeSH Terms | |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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