Suppression of Tie-1 in endothelial cells in vitro induces a change in the genome-wide expression profile reflecting an inflammatory function

被引:17
作者
Chan, Barden [1 ]
Sukhatme, Vikas P. [1 ]
机构
[1] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Interdisciplinary Med & Biotechnol,Dept Med, Boston, MA 02215 USA
来源
FEBS LETTERS | 2009年 / 583卷 / 06期
关键词
Tie-1; Endothelial inflammation; Microarray; U937; E-DEFICIENT MICE; RHEUMATOID-ARTHRITIS; SYNOVIAL TISSUE; ATHEROSCLEROSIS; INTERLEUKIN-1; PROTEIN; SITES; CD137; FLOW;
D O I
10.1016/j.febslet.2009.02.027
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Tie-1 is an endothelial specific receptor tyrosine kinase that is upregulated in diseases such as atherosclerosis and rheumatoid arthritis. We recently demonstrated that Tie-1 induced a proinflammatory response when overexpressed in endothelial cells. Here, we used a complementary approach and suppressed endogenous Tie-1 expression in endothelial cells to examine its function by microarray analysis. Tie-1 appeared to govern expression of many genes involved in inflammation. Expression knockdown of Tie-1 significantly reduced endothelial conditioned medium ability to stimulate MCP-1 production in U937 cells. Collectively, our results support the notion that Tie-1 has an inflammatory function in endothelial cells. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码:1023 / 1028
页数:6
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