TAILIEUCHUNG - Báo cáo khoa học: Overexpression of Tfam protects mitochondria against b-amyloid-induced oxidative damage in SH-SY5Y cells

There is strong evidence thatb-amyloid (Ab) causes oxidative stress and induces mitochondrial dysfunction in the pathogenesis of Alzheimer’s dis-ease. Mitochondrial transcription factor A (Tfam) has multiple roles in the maintenance of mtDNA. To study the protective roles of Tfam against amyloid neurotoxicity, we established SH-SY5Y cell lines stably over-expressing Tfam and exposed them to 10lmAb1-42 for 24 h. | ễFEBS Journal Overexpression of Tfam protects mitochondria against b-amyloid-induced oxidative damage in SH-SY5Y cells Shangcheng Xu Min Zhong Lei Zhang Yuan Wang Zhou Zhou Yutong Hao Wenyan Zhang Xuesen Yang Aimin Wei Liping Pei and Zhengping Yu Department of OccupationalHealth Third Military MedicalUniversity Chongqing China Keywords Alzheimer s disease mitochondrial transcription factor A mtDNA oxidative stress b-amyloid Correspondence Z. Yu Department of Occupational Health Third Military MedicalUniversity Gaotanyan Street Shapingba District Chongqing 400038 China Fax 86 23 6875 2290 Tel 86 23 6875 2290 E-mail yuzping@ These authors contributed equally to this study Received 5 March 2009 revised 13 April 2009 accepted 13 May 2009 doi There is strong evidence that b-amyloid Ab causes oxidative stress and induces mitochondrial dysfunction in the pathogenesis of Alzheimer s disease. Mitochondrial transcription factor A Tfam has multiple roles in the maintenance of mtDNA. To study the protective roles of Tfam against amyloid neurotoxicity we established SH-SY5Y cell lines stably overexpressing Tfam and exposed them to 10 IM Ab1-42 for 24 h. We found that Tfam overexpression attenuated Ab1-42-induced cell viability damage and apoptosis. In addition Tfam overexpression significantly suppressed the increase in excess reactive oxygen species and reversed the reduction in cytochrome c oxidase activity and ATP production induced by Ab 1-42. Furthermore overexpression of AC-Tfam which has no functional domain for stimulating mtDNA transcription but can still maintain the mtDNA nucleoid formation and mtDNA copy number also exhibited protective effects against Ab1-42 cytotoxicity in SH-SY5Y cells. Together our data suggest that Tfam overexpression protects mitochondria against Ab-induced oxidative damage in SH-SY5Y cells. These beneficial effects may be attributable to the roles of Tfam in maintaining mtDNA nucleoid formation

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