FXIII und endotheliale Barrierenfunktion

Th. Noll; G. Wozniak

doi:10.1055/s-0037-1622010

Hämostaseologie, Table of Contents

Hamostaseologie 2002; 22(01): 14-17
DOI: 10.1055/s-0037-1622010

Original Article

Schattauer GmbH

FXIII und endotheliale Barrierenfunktion

Factor XIII and endothelial barrier function

Authors

Th. Noll

¹Physiologisches Institut, Justus-Liebig-Universität Gießen (Leiter: Prof. Dr. Dr. H. M. Piper)
G. Wozniak

²Klinik für Gefäßchirurgie, Knappschaftskrankenhaus Bottrop (Leiter: Priv.-Doz. Dr. med. G. Wozniak)

Abstract

Zusammenfassung

Die Plasmatransglutaminase FXIIIa (FXIIIa) vernetzt Fibrinmonomere zu einem stabilen Thrombus. Aufgrund dieser Eigenschaft spielt der FXIIIa eine bedeutende Rolle bei der Blutgerinnung und Fibrinolyse. Darüber hinaus ist bereits lange bekannt, dass FXIIIa auch an Zelladhäsion und Migration, Aufbau der extrazellulären Matrix, Gewebereparatur und Wundheilung beteiligt ist. Neue experimentelle Befunde zeigen, dass FXIIIa die endotheliale Schranke stabilisieren kann. Dabei reduziert FXIIIa die Makromolekülpermeabilität in kultivierten Endothelzellschichten und verhindert ein drohendes Schrankenversagen (z. B. während Ischämie-Reperfusion) im Koronarsystem des isolierten Herzens. Diese Wirkung auf die endotheliale Schrankenfunktion wird der Eigenschaft des FXIIIa zugeschrieben, eine Reihe von Proteinen zu vernetzen, die in der extrazellulären Matrix im Bereich der interendothelialen Spalten vorkommen.

Summary

Activated factor XIII (FXIIIa) crosslinks fibrin monomers to a stable clot. Due to this function, FXIIIa plays a major role in hemostasis and fibrinolysis. Additionally, it is well known that FXIIIa has a special meaning in cell adhesion and migration, in generation of extracellular matrix, in tissue repair and wound healing. New experimental studies revealed a FXIIIa stabilizing endothelial barrier function. In this function, FXIIIa reduces endothelial permeability for macromolecules in cultured endothelial monolayers and prevents impending barrier failure in coronary arteries of isolated hearts. This effect is due to the cross-linking of several proteins within the extracellular matrix, especially in the interendothelial clefts.

Schlüsselwörter

Endothel - Schrankenfunktion - Ischämie-Reperfusion - Langendorff-Perfusion

Keywords

Endothelial monolayer - stabilization of barrier function - ischemia reperfusion - Langendorff circuit

Full Text

References

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