TAILIEUCHUNG - Báo cáo khoa học: Glycogen synthase kinase 3b and b-catenin pathway is involved in toll-like receptor 4-mediated NADPH oxidase 1 expression in macrophages

Macrophage activation contributes to the pathogenesis of atherosclerosis. In the vascular system, the major source of reactive oxygen species is the NADPH oxidase (Nox) family. Nox1 is induced by lipopolysaccharide (LPS) in macrophages, but the expression mechanism is not fully under-stood. | Glycogen synthase kinase 3b and b-catenin pathway is involved in toll-like receptor 4-mediated NADPH oxidase 1 expression in macrophages Jin-Sik Kim1 Seungeun Yeo1 Dong-Gu Shin2 Yoe-Sik Bae3 Jae-Jin Lee4 Byung-Rho Chin4 Chu-Hee Lee1 and Suk-Hwan Baek1 1 Department of Biochemistry Molecular Biology Yeungnam University Daegu Korea 2 Department of InternalMedicine Yeungnam University Daegu Korea 3 Department of Biochemistry Dong-A University Busan Korea 4 Department of Dentistry Yeungnam University Daegu Korea Keywords glycogen synthase kinase 3p NADPH oxidase 1 reactive oxygen species toll-like receptor 4 b-catenin Correspondence Suk-Hwan Baek Department of Biochemistry Molecular Biology College of Medicine Yeungnam University 317-1 Daemyung-5 Dong Daegu 705-717 Korea Fax 82 53 623 8032 Tel 82 53 620 4523 E-mail sbaek@ These authors contributed equally to this work Received 25 February 2010 revised 23 April 2010 accepted 27 April 2010 Macrophage activation contributes to the pathogenesis of atherosclerosis. In the vascular system the major source of reactive oxygen species is the NADPH oxidase Nox family. Nox1 is induced by lipopolysaccharide LPS in macrophages but the expression mechanism is not fully understood. We found that LPS causes b-catenin accumulation by glycogen synthase kinase 3 b GSK3b inactivation and that b-catenin accumulation increases Nox1 expression. LPS induced Nox1 mRNA expression and reactive oxygen species generation in cells. Using bone marrow-derived macrophages from toll-like receptor 4 mutant mice we also tested whether LPS-induced Nox1 expression is toll-like receptor 4 dependent. LPS caused GSK3b phosphorylation induced b-catenin accumulation and increased nuclear translocation. The GSK3b inhibitor LiCl potentiated LPS-induced Nox1 expression in accordance with b-catenin accumulation and nuclear translocation. Conversely ectopic expression of a constitutively active GSK3b mutant severely attenuated Nox1 expression. .

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