The antioxidant function of Bcl-2 preserves cytoskeletal stability of cells with defective respiratory complex I |
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Authors: | A M Porcelli A Ghelli L Iommarini E Mariani M Hoque C Zanna G Gasparre M Rugolo |
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Institution: | (1) Dipartimento di Biologia Evoluzionistica Sperimentale, Università di Bologna, Via Irnerio 42, Bologna, 40122, Italy;(2) Unità di Genetica Medica, Policlinico Universitario S.Orsola-Malpighi, Università di Bologna, Bologna, 40138, Italy |
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Abstract: | Human thyroid carcinoma XTC.UC1 cells harbor a homoplasmic frameshift mutation in the MT-ND1 subunit of respiratory complex
I. When forced to use exclusively oxidative phosphorylation for energy production by inhibiting glycolysis, these cells triggered
a caspase-independent cell death pathway, which was associated to a significant imbalance in glutathione homeostasis and a
cleavage of the actin cytoskeleton. Overexpression of the anti-apoptotic Bcl-2 protein significantly increased the level of
endogenous reduced glutathione, thus preventing its oxidation after the metabolic stress. Furthermore, Bcl-2 completely inhibited
actin cleavage and increased cell adhesion, but was unable to improve cellular viability. Similar effects were obtained when
XTC.UC1 cells were incubated with exogenous glutathione. We hence propose that Bcl-2 can safeguard cytoskeletal stability
through an antioxidant function.
Received 28 May 2008; received after revision 8 July 2008; accepted 29 July 2008 |
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Keywords: | " target="_blank"> Mitochondria Bcl-2 cytoskeleton glutathione complex I |
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