A disintegrin and metalloproteinase with thrombospondin motif 1(ADAMTS1) expression increases in acute aortic dissection

查看全文 作　　者：Yanxiang [1]Gao;Wenjing [1]Wu;Changan [2]Yu;Fangming [1]Zhong;Geng [2]Li;Wei [3]Kong;Jingang [1]Zheng

机构地区：[1]Department of Cardiology, China-Japan Friendship Hospital;[2]Central Laboratory of Cardiovascular Disease, China-Japan Friendship Hospital;[3]Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University

出　　处：《Science China(Life Sciences)》索引2016年第59卷第1期,共9页

基　　金：supported by the National Natural Science Foundation of China(81170287) 摘　　要：Acute aortic dissection(AAD) is a life-threatening cardiovascular disease caused by progressive medial degeneration of the aortic wall. A disintegrin and metalloproteinase with thrombospondin motifs 1(ADAMTS1) is a recently identified extracellular metalloproteinase participating in the development of vascular disease, such as atherosclerosis. In the present study, we found that ADAMTS1 was significantly elevated in blood samples from AAD patients compared with patients with acute myocardial infarction and healthy volunteers. Based on these findings, we established an AAD model by infusing angiotensin II in older mice. AAD was successfully developed in aorta tissues, with an incidence of 42% after 14 days in the angiotensin II group. Macrophage and neutrophil infiltration was observed in the media of the aorta, and ADAMTS1 overexpression was found in the aorta by Western blot and immunohistochemistry. Double immunofluorescence staining showed the expression of ADAMTS1 in macrophages and neutrophils. Consistent with the upregulation of ADAMTS1 in aortic dissection tissues, versican(a proteoglycan substrate of ADAMTS1) was degraded significantly more in these tissues than in control aortic tissues. These data suggest that the increased expression of ADAMTS1 protein in macrophages and neutrophils that infiltrated aortic tissues may promote the progression of AAD by degrading versican. 关键词：基质金属蛋白酶急性心肌梗死主动脉去整合素血小板夹层免疫组织化学血管紧张素II

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A disintegrin and metalloproteinase with thrombospondin motif 1(ADAMTS1) expression increases in acute aortic dissection

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