Genistein enhances the ICAM-mediated adhesion by inducing the expression of ICAM-1 and its counter-receptors

Biochemical and Biophysical Research Communications
S TiisalaR Renkonen

Abstract

Binding of circulating cells to endothelium is mediated by recognition between endothelial adhesion molecules and their counter-receptors. The beta 2 integrins are a group of adhesion molecules, mainly expressed on leukocytes, that mediate intercellular binding by recognizing their counterparts on endothelial cells, among others ICAM-1. In this study we have studied the regulation of this interaction in myelomonocytic cells treated with genistein, a tyrosine kinase inhibitor with several other biological functions. We show that genistein upregulates the surface expression of the beta 2-integrins in the monoblastic THP-1 and to a lesser extent in the promyelocytic HL-60 leukemia cell lines. This upregulation leads to an increase in the adherence of THP-1 cells to ICAM-1. Genistein also modulates the expression of ICAM-1 on endothelial cells by potentiating the upregulating effect of TNF and IFN-gamma. Genistein may thus enhance intercellular binding by affecting both the endothelium and the circulating cells.

Citations

Jun 13, 1998·International Journal of Urology : Official Journal of the Japanese Urological Association·K GriffithsM S Morton
Jun 10, 2008·Toxicology Letters·Shannan RodriguezElizabeth Hong-Geller
Jun 29, 1999·Baillière's Clinical Endocrinology and Metabolism·K GriffithsM S Morton
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Apr 5, 2005·American Journal of Physiology. Heart and Circulatory Physiology·Balu K ChackoRakesh P Patel
Mar 5, 1998·The American Journal of Physiology·S A KellyG B Bulkley

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