THROMBIN-INDUCED GAP FORMATION IN CONFLUENT ENDOTHELIAL-CELL MONOLAYERS INVITRO

Google Scholar
  • 1 January 1983
    • journal article
    • research article
    • Vol. 62  (3) , 549-556
Abstract
When thrombin is incubated with confluent monolayer of human umbilical vein endothelial cells in vitro, there is a change in the shape of the endothelial cells that results in gaps in the monolayer, disrupting the integrity of the endothelium and exposing the subendothelium. Using a grid assay to measure this phenomenon, it was observed that up to 80% of the surface area once covered by cells was uncovered after a 15-min incubation with 10-2 U/ml(10-10 M) thrombin. The effect was apparent within 2 min and did not remove cells from the surface of the culture dish. The gaps in the monolayer completely disappeared within 2 h after exposure to thrombin. The effect of thrombin was inhibited by preincubation of thrombin with hirudin or antithrombin III plus heparin or by preincubation of the monolayers with dibutyryl cAMP (dbcAMP). Histamine also induced gap formation in endothelial cell monolayers. Both pyrilamine and cimetidine prevented the histamine-induced effect, but they had no effect on thrombin-induced gap formation. Intact monolayers were not disrupted by bradykinin, serotonin, C5a or C3a. Evidently, small amounts of thrombin can induce repeated and transient exposure of the subendothelium, a situation believed to be conducive to antherogenesis and thrombosis.

This publication has 3 references indexed in Scilit: