Hypertensive Versus Normotensive Monocyte Adhesion to Cultured Cerebral Microvascular Endothelial Cells

  • R. M. McCarron
  • Y. Yoshihide
  • M. Spatz
  • J. Hallenbeck
Part of the Advances in Behavioral Biology book series (ABBI, volume 46)

Summary

Hypertension may predispose to the development of thrombotic vascular disease by promoting interactions between circulating blood monocytes (mo) and vascular endothelial cells (EC). The adherence of mo from spontaneously hypertensive (SHR), normotensive Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats to cultures of activated and untreated homologous cerebral microvascular EC was examined. There were no significant differences in the percent of monocytes from all three strains adhering to untreated EC. Mo binding was inhibited (approx. 50%) by antibodies against (β2-integrin molecules (CD 11 a, CD 11 b, CD l 8) and intercellular adhesion molecule-1 (ICAM-l). Treatment of EC with LPS, IL–1β, TNFα or IFNγ dose-dependently upregulated mo adhesion. The level of syngeneic and allogeneic mo adhesion to stimulated SHR EC was significantly more upregulated than was observed with identically treated WKY or SD EC (p<0.001). Mo adhesion to stimulated EC was inhibited (10–20%) by antibodies to the β1-integrin, VLA-4 and antibodies to the β2-integrins and ICAM-1 (20–25%). These results demonstrated that treated SHR EC exhibited significantly higher adhesivity and suggest that hypertension may enhance responsiveness of endothelium to factors which promote mo adhesion. Subsequent mo interactions, via cytokines, may be important in the genesis of stroke.

Keywords

Monocyte Adhesion Endothelial Cell Monolayer Cerebral Microvascular Endothelial Cell Cerebrovascular Endothelial Cell Circulate Blood Monocyte 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Résumé

L’hypertension artérielle peutr favoriser l’interaction des monocytes circulants (Mo) avec les cellules endothéliales des vaisseaux sanguins (CE) et ainsi prédisposer au développement de la thrombose vasculaire. Afin d’étudier ce phénomène, nous avons examiné l’adhérence des Mo issus de rats présentant une hypertension spontanée (souche SHR) et de rat normotendus (Wistar-Kyoto WKY et Sprague-Dawley SD) sur des cultures de cellules endothéliales microvasculaires homologues activées ou non. Le nombre de Mo adhérant sur les cultures de cellules endothéliales est identique, quelle que soit la souche de rats étudiée. L’interaction des Mo est inhibée à 50% par les anticorps anti-b2-intégrine (CD1 1 a, CD 11 b, CD18) et par la molécule d’adhésion intercellulaire ICAM-1.Le traitement des CE par le LPS, l’IL-lb, le TNFa ou l’IFNg augmente l’adhésion des Mo de façon dose-dépendante. Cette induction de l’interaction des Mo syngéniques et allogéniques sur des cultures d’EC stimulées de rats SHR est plus importante que celle observée avec des cultures d’EC stimulées de rats WKY ou SD (P). L’interaction entre les Mo et les EC stimulées est inhibée par des anticorps anti-intégrine-bl, VLA-4 (10–20%) et par des anticorps anti-intégrine-b2 ou l’ICAM-1 (20–25%). Ces résultats montrent que des cultures de cellules endothéliales microvasculaires de rats SHR présentent une plus grande adhésivité, et suggèrent que l’hypertension pourrait induire la réponse de l’endothélium vasculaire à des facteurs promouvant l’adhésion des monocytes. De telles interactions, par l’intermédiaire de cytokines, peuvent jouer un rôle important dans la genèse des thromboses cérébrales.

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Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  • R. M. McCarron
    • 1
  • Y. Yoshihide
    • 1
  • M. Spatz
    • 1
  • J. Hallenbeck
    • 1
  1. 1.Stroke Branch, NINDSNIHBethesdaUSA

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