Differential effects of histamine and thrombin on endothelial barrier function through actin-myosin tension

1  Department of Internal Medicine and 2  Department of Biomedical Engineering, University of Iowa, Iowa City, Iowa 52242 We compared temporal changes in isometric tension in cultured human umbilical vein endothelial cells inoculated on a polymerized collagen membrane with changes in cell-cell and c...

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Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 2002-01, Vol.282 (1), p.H21-H29
Main Authors: Moy, Alan B, Blackwell, Ken, Kamath, Anant
Format: Article
Language:English
Subjects:
Actins - metabolism
Cells, Cultured
Endothelium, Vascular - drug effects
Endothelium, Vascular - physiology
Histamine - pharmacology
Humans
Isometric Contraction - drug effects
Isometric Contraction - physiology
Kinetics
Myosins - metabolism
Thrombin - pharmacology
Umbilical Veins
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Summary:1  Department of Internal Medicine and 2  Department of Biomedical Engineering, University of Iowa, Iowa City, Iowa 52242 We compared temporal changes in isometric tension in cultured human umbilical vein endothelial cells inoculated on a polymerized collagen membrane with changes in cell-cell and cell-matrix adhesion derived by a mathematical model of transendothelial cell resistance. Thrombin and histamine disrupt barrier function by targeting a greater loss in cell-cell adhesion, which preceded losses in overall transendothelial resistance. There were minor losses in cell-matrix adhesion, which was temporally slower than the decline in the overall transendothelial resistance. In contrast, thrombin and histamine restored barrier function by initiating a restoration of cell-matrix adhesion, which occurred before an increase in overall transendothelial resistance. Thrombin mediated a second and slower decline in cell-cell adhesion, which was not observed in histamine-treated cells. This decline in cell-cell adhesion temporally correlated with expressed maximal levels of tension development, suggesting that actin-myosin contraction directly strains cell-cell adhesion sites. Pretreatment of cells with ML-7 mediated more rapid recovery of cell-cell adhesion and had no effect on cell-matrix adhesion. Taken together, expression of actin-myosin contraction affects the restoration of barrier function by straining cell-cell adhesion sites. electrical resistance; analytic modeling
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.2002.282.1.h21