TAILIEUCHUNG - Báo cáo khoa học: Increased expression of c-Fos by extracellular signal-regulated kinase activation under sustained oxidative stress elicits BimEL upregulation and hepatocyte apoptosis

We previously reported that the inhibition of catalase and glutathione per-oxidase activities by treatment with 3-amino-1,2,4-triazole (ATZ) and mer-captosuccinic acid evoked sustained increases in the levels of reactive oxygen species and apoptosis in rat primary hepatocytes. | 1FEBS Journal Increased expression of c-Fos by extracellular signal-regulated kinase activation under sustained oxidative stress elicits BimEL upregulation and hepatocyte apoptosis Yasuhiro Ishihara1 Fumiaki Ito2 and Norio Shimamoto1 1 Laboratory of Pharmacology Faculty of PharmaceuticalSciences at Kagawa Tokushima Bunri University Japan 2 Department of Biochemistry Faculty of PharmaceuticalSciences Setsunan University Osaka Japan Keywords apoptosis Bim c-Fos extracellular signal-regulated kinase ERK reactive oxygen species Correspondence N. Shimamoto Laboratory of Pharmacology Faculty of Pharmaceutical Sciences at Kagawa Tokushima Bunri University 1314-1 Shido Sanuki Kagawa 769-2193 Japan Fax 81 87 894 0181 Tel 81 87 894 5111 ext. 6513 E-mail n-shimamoto@ Received 22 December 2010 revised 25 February 2011 accepted 22 March 2011 doi We previously reported that the inhibition of catalase and glutathione peroxidase activities by treatment with 3-amino-1 2 4-triazole ATZ and mercaptosuccinic acid evoked sustained increases in the levels of reactive oxygen species and apoptosis in rat primary hepatocytes. Apoptosis was accompanied by increased expression of BimEL following activation of extracellular signal-regulated kinase. The aim of this study was to characterize the mechanism underlying hepatocyte apoptosis by identifying the transcription factor that induces BimEL expression. The bim promoter region was cloned into a promoterless-luc vector and promoter activity was monitored by a luciferase assay. The luciferase activity increased in the presence of ATZ mercaptosuccinic acid. Pretreatment with a MEK inhibitor U0126 or an antioxidant vitamin C suppressed the promoter activity. Furthermore ATZ mercaptosuccinic acid-induced luciferase activity was attenuated by mutation of the activator protein-1 binding site in the bim promoter region. The amounts of total and phosphorylated c-Fos increased over time in the presence

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