Digitale Bibliotheek
Sluiten Bladeren door artikelen uit een tijdschrift
 
<< vorige    volgende >>
     Tijdschrift beschrijving
       Alle jaargangen van het bijbehorende tijdschrift
         Alle afleveringen van het bijbehorende jaargang
           Alle artikelen van de bijbehorende aflevering
                                       Details van artikel 3 van 6 gevonden artikelen
 
 
  Low shear stress regulates monocyte adhesion to oxidized lipid-induced endothelial cells via an IkappaBalpha dependent pathway
 
 
Titel: Low shear stress regulates monocyte adhesion to oxidized lipid-induced endothelial cells via an IkappaBalpha dependent pathway
Auteur: Chu-hong Zhu
Da-jun Ying
Jian-hong Mi
Xing-hong Zhu
Jian-sen Sun
Xiao-ping Cui
Verschenen in: Biorheology
Paginering: Jaargang 41 (2004) nr. 2 pagina's 127-137
Jaar: 2004-03-31
Inhoud: In regions of a vessel that experience low shear stress and reversing flow patterns, early features in the pathogenesis of atherosclerosis include the accumulation of oxidized LDL (OxLDL) and adhesion of monocytes to endothelial cells (EC). Here we investigated the hypothesis that low shear stress (2 dyn/cm2) and OxLDL are synergistic for enhanced expression of vascular cell adhesion molecule (VCAM-1) and human aortic endothelial cell (HAEC)-monocyte adhesion. This study shows low shear stress can significantly reduce IkappaBalpha levels, activate NF-kappaB, increase the expression of VCAM-1 in HAEC and binding of monocytes. OxLDL itself cannot significantly increase the expression of VCAM-1 in HAEC and binding of monocytes, but through activation of NF-kappaB and degradation of IkappaBalpha induced by low shear stress it can significantly enhance VCAM-1 expression and monocyte adhesion, over that in unmodified LDL or control. These results suggest that low shear stress can regulate monocyte adhesion to oxidized lipid-induced endothelial cells via an IkappaBalpha-dependent pathway, and that low shear stress together with OxLDL may likely play an important role in atherogenesis.
Uitgever: IOS Press
Bronbestand: Elektronische Wetenschappelijke Tijdschriften
 
 

                             Details van artikel 3 van 6 gevonden artikelen
 
<< vorige    volgende >>
 
 Koninklijke Bibliotheek - Nationale Bibliotheek van Nederland