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Suppression of Tie‐1 in endothelial cells in vitro induces a change in the genome‐wide expression profile reflecting an inflammatory function
Author(s) -
Chan Barden,
Sukhatme Vikas P.
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.02.027
Subject(s) - proinflammatory cytokine , downregulation and upregulation , microbiology and biotechnology , inflammation , gene knockdown , function (biology) , microarray analysis techniques , endothelial stem cell , u937 cell , biology , in vitro , cancer research , immunology , gene expression , cell culture , gene , genetics
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.