Arginase I Attenuates Inflammatory Cytokine Secretion Induced by Lipopolysaccharide in Vascular Smooth Muscle Cells

被引:53
作者
Wang, Xu-ping [1 ,2 ]
Chen, Yu-guo [1 ,2 ]
Qin, Wei-dong [1 ,2 ]
Zhang, Wei [1 ,2 ]
Wei, Shu-jian [1 ,2 ]
Wang, Juan [1 ,2 ]
Liu, Fu Qiang [3 ]
Gong, Lei [3 ]
An, Feng Shuang [1 ,2 ]
Zhang, Yun [1 ,2 ]
Chen, Zhe-Yu [4 ]
Zhang, Ming-Xiang [1 ,2 ]
机构
[1] Shandong Univ, Qilu Hosp, Chinese Minist Educ, Key Lab Cardiovasc Remodeling & Funct Res, Jinan 250012, Shandong, Peoples R China
[2] Shandong Univ, Qilu Hosp, Chinese Minist Publ Hlth, Jinan 250012, Shandong, Peoples R China
[3] Shandong Univ, Qilu Hosp, Dept Endocrinol, Jinan 250012, Shandong, Peoples R China
[4] Shandong Univ, Sch Med, Dept Neurobiol, Shandong Prov Key Lab Mental Disorders, Jinan 250012, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
atherosclerosis; vascular biology; vascular muscle; NITRIC-OXIDE SYNTHASE; ATHEROSCLEROSIS; EXPRESSION; DISEASE; PEROXYNITRITE; SUPEROXIDE; INCREASES; MICE;
D O I
10.1161/ATVBAHA.111.229302
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective-Inflammation plays an important role in atherosclerosis. Arginase I (Arg I) promotes the proliferation of vascular smooth muscle cells; however, the effect of Arg I on inflammation remains unknown. The present study investigated the role of Arg I in inflammation in vitro and in vivo. Methods and Results-Quantitative reverse transcription-polymerase chain reaction and Western blot analysis demonstrated that Arg I inhibited tumor necrosis factor-alpha production induced by lipopolysaccharide in human aortic smooth muscle cells. Inducible nitric oxide synthase substrate competition and nuclear factor-kappa B activation were main contributors to lipopolysaccharide-mediated inflammatory cytokine generation. However, Arg I could attenuate the function of inducible nitric oxide synthase and inhibit the subsequent nuclear factor-kappa B activation, leading to inhibition of tumor necrosis factor-alpha generation. Furthermore, upregulation of Arg I significantly decreased macrophage infiltration and inflammation in atherosclerotic plaque of rabbits, whereas downregulation of Arg I aggravated these adverse effects. Conclusion-The results indicate the antiinflammatory effects of Arg I and suggest an unexpected beneficial role of Arg I in inflammatory disease. (Arterioscler Thromb Vasc Biol. 2011;31:1853-1860.)
引用
收藏
页码:1853 / 1860
页数:8
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