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© The Rockefeller University Press, 0022-1007/1999/5/1373/ $5.00
The Journal of Experimental Medicine, Volume 189, Number 9, May 3, 1999 1373-1382

Articles

Effect of Factor XIII on Endothelial Barrier Function

Thomas Noll*, Gernold Wozniak{ddagger}, Karin McCarson*, Amir Hajimohammad*, Hubert J. Metzner||, Javier Inserte*, Wolfgang Kummer§, Friedrich Wilhelm Hehrlein{ddagger}, and Hans Michael Piper*

From the * Physiologisches Institut, {ddagger} 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

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 x 10–6 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.

Key Words: edema • endothelial permeability • heart • ischemia-reperfusion • recombinant human factor XIII

Address correspondence to Thomas Noll, Physiologisches Institut, Justus-Liebig-Universität, Aulweg 129, D-35392 Giessen, Germany. Phone: 49-641-99-47243; Fax: 49-641-99-47239; E-mail: thomas.noll{at}physiologie.med.uni-giessen.de

Abbreviations used: DAB, 3,3'-diaminobenzidine; 2-DG, 2-deoxy-D-glucose; MI, metabolic inhibition; NCS, newborn calf serum.


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