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    Mechanisms of ER Stress-Mediated Mitochondrial Membrane Permeabilization.

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    Authors
    Gupta, Sanjeev
    Cuffe, Lorraine
    Szegezdi, Eva
    Logue, Susan E
    Neary, Catherine
    Healy, Sandra
    Samali, Afshin
    Affiliation
    Apoptosis Research Centre, School of Natural Sciences, National University of Ireland, Galway, Ireland.
    Issue Date
    2010
    
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    Citation
    Mechanisms of ER Stress-Mediated Mitochondrial Membrane Permeabilization. 2010, 2010:170215 Int J Cell Biol
    Journal
    International journal of cell biology
    URI
    http://hdl.handle.net/10147/93851
    DOI
    10.1155/2010/170215
    PubMed ID
    20169117
    Abstract
    During apoptosis, the process of mitochondrial outer membrane permeabilization (MOMP) represents a point-of-no-return as it commits the cell to death. Here we have assessed the role of caspases, Bcl-2 family members and the mitochondrial permeability transition pore on ER stress-induced MOMP and subsequent cell death. Induction of ER stress leads to upregulation of several genes such as Grp78, Edem1, Erp72, Atf4, Wars, Herp, p58ipk, and ERdj4 and leads to caspase activation, release of mitochondrial intermembrane proteins and dissipation of mitochondrial transmembrane potential (DeltaPsim). Mouse embryonic fibroblasts (MEFs) from caspase-9, -2 and, -3 knock-out mice were resistant to ER stress-induced apoptosis which correlated with decreased processing of pro-caspase-3 and -9. Furthermore, pretreatment of cells with caspase inhibitors (Boc-D.fmk and DEVD.fmk) attenuated ER stress-induced loss of DeltaPsim. However, only deficiency of caspase-9 and -2 could prevent ER stress-mediated loss of DeltaPsim. Bcl-2 overexpression or pretreatment of cells with the cell permeable BH4 domain (BH4-Tat) or the mitochondrial permeability transition pore inhibitors, bongkrekic acid or cyclosporine A, attenuated the ER stress-induced loss of DeltaPsim. These data suggest a role for caspase-9 and -2, Bcl-2 family members and the mitochondrial permeability transition pore in loss of mitochondrial membrane potential during ER stress-induced apoptosis.
    Language
    en
    ISSN
    1687-8884
    ae974a485f413a2113503eed53cd6c53
    10.1155/2010/170215
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