原创力文档regulation of ccl5 expression in smooth muscle cells following arterial injury监管ccl5表达在动脉损伤后平滑肌细胞.pdfVIP
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regulation of ccl5 expression in smooth muscle cells following arterial injury监管ccl5表达在动脉损伤后平滑肌细胞
Regulation of CCL5 Expression in Smooth Muscle Cells
Following Arterial Injury
1,2. 3. 1 3 4 1 3
Huan Liu , Huan Ning , Hongchao Men , Rong Hou , Mingui Fu , Hailin Zhang *, Jianguo Liu *
1 Department of Pharmacology, Hebei Medical University, Shijiazhuang, China, 2 Heibei North University Medical College, Zhangjiakou, China, 3 Division of Infectious
Diseases, Allergy and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, Missouri, United States of America, 4 Shock/
Trauma Research Center Department of Basic Medical Science, School of Medicine, University of Missouri Kansas City, Missouri, United States of America
Abstract
Chemokines play a crucial role in inflammation and in the pathophysiology of atherosclerosis by recruiting inflammatory
immune cells to the endothelium. Chemokine CCL5 has been shown to be involved in atherosclerosis progression. However,
little is known about how CCL5 is regulated in vascular smooth muscle cells. In this study we report that CCL5 mRNA
expression was induced and peaked in aorta at day 7 and then declined after balloon artery injury, whereas IP-10 and MCP-1
mRNA expression were induced and peaked at day 3 and then rapidly declined. The expression of CCL5 receptors (CCR1, 3
5) were also rapidly induced and then declined except CCR5 which expression was still relatively high at day 14 after
balloon injury. In rat smooth muscle cells (SMCs), similar as in aorta CCL5 mRNA expression was induced and kept increasing
after LPS plus IFN-gamma stimulation, whereas IP-10 mRNA expression was rapidly induced and then declined. Our data
further indicate that induction of CCL5 expression in SMCs was mediated by IRF-1 via bi
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