CYCLIC STRAIN ENHANCES ADHESION OF MONOCYTES TO ENDOTHELIAL-CELLS BY INCREASING INTERCELLULAR-ADHESION MOLECULE-1 EXPRESSION

Citation
Jj. Cheng et al., CYCLIC STRAIN ENHANCES ADHESION OF MONOCYTES TO ENDOTHELIAL-CELLS BY INCREASING INTERCELLULAR-ADHESION MOLECULE-1 EXPRESSION, Hypertension, 28(3), 1996, pp. 386-391
Citations number
36
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0194911X
Volume
28
Issue
3
Year of publication
1996
Pages
386 - 391
Database
ISI
SICI code
0194-911X(1996)28:3<386:CSEAOM>2.0.ZU;2-C
Abstract
Since endothelial cells are constantly subjected to pressure-induced s train, we examined how cyclic strain affects the expression of interce llular adhesion molecule-1 (ICAM-1). Endothelial cells grown on a flex ible membrane base were deformed by different sinusoidal negative pres sures (-10, -15, or -20 kPa) to produce an average strain of 9%, 11%, and 12%, respectively, for various times, The release of the soluble f orm of ICAM-1 from strained endothelial cells increased in a time- and strain-dependent manner. Using flow cytometric analysis, we showed th e induction of ICAM-1 expression on the endothelial cell surface to de pend on both time and the amount of strain. Northern blot analysis rev ealed a sustained, approximately 1.8-fold increase in ICAM-1 mRNA leve ls in 11% strained cells. Strain-induced expression of ICAM-1 correlat ed with a strain-dependent increase in adhesion of monocytic cells to strained cells. This increase in monocytic cell adhesion could be part ially inhibited by pretreatment of strained cells with antibody to ICA M-1. These results indicate that mechanical strain can stimulate the e xpression of ICAM-1 by endothelial cells and thus contribute tu the in creased adhesion of monocytes to strained cells. Such strain-induced e xpression of ICAM-1 may contribute to the trapping of monocytes on loc al vascular walls where strain is high and to the initiation of athero genesis, thus providing a possible link between hypertension and ather ogenesis.