FEBS Letters
Volume 583, Issue 6 , Pages 1023-1028, 18 March 2009

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

Edited by Giulio Superti-Furga

Division of Interdisciplinary Medicine and Biotechnology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, RW 563, Boston, MA 02215, United States

Received 19 November 2008; received in revised form 4 February 2009; accepted 18 February 2009. published online 24 February 2009.

Abstract 

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.

Abbreviation: HUVEC, human umbilical vein endothelial cell

Keywords: Tie-1, Endothelial inflammation, Microarray, U937

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PII: S0014-5793(09)00138-0

doi:10.1016/j.febslet.2009.02.027

FEBS Letters
Volume 583, Issue 6 , Pages 1023-1028, 18 March 2009