o-glcnac modification of nfκb p65 inhibits tnf-α-induced inflammatory mediator expression in rat aortic smooth muscle cellso-glcnac修改nfκb p65抑制tnf-α-induced炎性介质表达鼠主动脉平滑肌细胞.pdfVIP

O-GlcNAc Modification of NFkB p65 Inhibits TNF-a-Induced Inflammatory Mediator Expression in Rat Aortic Smooth Muscle Cells 1 . 1,4. 1 2 1 Dongqi Xing * , Kaizheng Gong , Wenguang Feng , Susan E. Nozell , Yiu-Fai Chen , John C. Chatham3, Suzanne Oparil1 1Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 2 Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 3 Division of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 4 Division of Cardiovascular Disease, Department of Medicine, Yangzhou University, Yangzhou, Jiangsu, China Abstract Background: We have shown that glucosamine (GlcN) or O-(2-acetamido-2-deoxy-D-glucopyranosylidene)amino-N- phenylcarbamate (PUGNAc) treatment augments O-linked-N-acetylglucosamine (O-GlcNAc) protein modification and attenuates inflammatory mediator expression, leukocyte infiltration and neointima formation in balloon injured rat carotid arteries and have identified the arterial smooth muscle cell (SMC) as the target cell in the injury response. NFkB signaling has been shown to mediate the expression of inflammatory genes and neointima formation in injured arteries. Phosphorylation of the p65 subunit of NFkB is required for the transcriptional activation of NFkB. This study tested the hypothesis that GlcN or PUGNAc treatment protects vascular SMCs against tumor necrosis factor (TNF)-a induced inflam