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J. Exp. Med.,
Volume 189, Number 9, May 3, 1999 1373-1382
By
From the * Physiologisches Institut, The effect of factor XIII on endothelial barrier function was studied in a model of cultured
monolayers of porcine aortic endothelial cells and saline-perfused rat hearts. The thrombin-activated plasma factor XIII (1 U/ml) reduced albumin permeability of endothelial monolayers
within 20 min by 30 ± 7% (basal value of 5.9 ± 0.4 × 10 Klinik für Herz- und Gefässchirurgie, § Institut für Anatomie und
Zellbiologie, Justus-Liebig-Universität, D-35392 Giessen, Germany; and Centeon Pharma GmbH,
D-35001 Marburg, Germany
6 cm/s), whereas the nonactivated
plasma factor XIII had no effect. Reduction of permeability to the same extent, i.e., by 34 ± 9% could be obtained with the thrombin-activated A subunit of factor XIII (1 U/ml), whereas the
iodoacetamide-inactivated A subunit as well as the B subunit had no effect on permeability.
Endothelial monolayers exposed to the activated factor XIII A exhibited immunoreactive deposition of itself at interfaces of adjacent cells; however, these were not found on exposure to
nonactivated factor XIII A or factor XIII B. Hyperpermeability induced by metabolic inhibition (1 mM potassium cyanide plus 1 mM 2-deoxy-D-glucose) was prevented in the presence
of the activated factor XIII A. Likewise, the increase in myocardial water content in ischemic-reperfused rat hearts was prevented in its presence. This study shows that activated factor XIII
reduces endothelial permeability. It can prevent the loss of endothelial barrier function under
conditions of energy depletion. Its effect seems related to a modification of the paracellular passageways in endothelial monolayers.
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