TAILIEUCHUNG - Báo cáo khoa học: Analysis of oxidative events induced by expanded polyglutamine huntingtin exon 1 that are differentially restored by expression of heat shock proteins or treatment with an antioxidant

We recently reported that the transient expression of polyglutamine tracts of various size in exon 1 of the huntingtin polypeptide (httEx1) generated abnormally high levels of intracellular reactive oxygen species that directly contributed to cell death. Here, we compared the protection generated by heat shock proteins to that provided by the antioxidant agentN-acetyl-l-cysteine. | iFEBS Journal Analysis of oxidative events induced by expanded polyglutamine huntingtin exon 1 that are differentially restored by expression of heat shock proteins or treatment with an antioxidant Wance J. J. Firdaus1 Andreas Wyttenbach2 Chantal Diaz-Latoud1 R. W. Currie1 3 and Andre-Patrick Arrigo1 1 Laboratoire Stress Oxydant Chaperons et Apoptose Centre de Genetique Moleculaire et Cellulaire Universite Claude Bernard Lyon-1 Villeurbanne France 2 Southampton Neuroscience Group Schoolof BiologicalSciences University of Southampton UK 3 Department of Anatomy and Neurobiology Dalhousie University Halifax Canada Keywords heat shock proteins huntingtin polyQ inclusion bodies oxidized proteins proteasome reactive oxygen species Correspondence . Arrigo Laboratoire Stress Oxydant Chaperons et Apoptose CNRS UMR 5534 Centre de Genetique Moleculaire et Cellulaire Universite Claude Bernard Lyon-1 43 Blvd du 11 Novembre 69622 Villeurbanne Cedex France Fax 33 472 440555 Tel 33 472 432685 E-mail arrigo@ Received 16 February 2006 revised 20 April2006 accepted 12 May 2006 doi We recently reported that the transient expression of polyglutamine tracts of various size in exon 1 of the huntingtin polypeptide httExl generated abnormally high levels of intracellular reactive oxygen species that directly contributed to cell death. Here we compared the protection generated by heat shock proteins to that provided by the antioxidant agent N-acetyl-L-cysteine. In cells expressing httEx1 with 72 glutamine repeats httEx1-72Q the overexpression of Hsp27 or Hsp70 plus Hdj-1 Hsp40 or treatment of the cells with N-acetyl-L-cysteine inhibited not only mitochondrial membrane potential disruption but also the increase in reactive oxygen species nitric oxide and protein oxidation. However only heat shock proteins and not N-acetyl-L-cysteine reduced the size of the inclusion bodies formed by httEx1-72Q. In cells expressing httEx1 polypeptide with 103

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