VEGF released from a fibrin biomatrix increases VEGFR-2 expression and improves early outcome after ischaemia-reperfusion injury.

Moritz, Martina; Pfeifer, Sabine; Balmayor, Elizabeth R; Mittermayr, Rainer; Wolbank, Susanne; Redl, Heinz; Van Griensven, Martijn

doi:10.1002/term.2114

2017

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Title:: VEGF released from a fibrin biomatrix increases VEGFR-2 expression and improves early outcome after ischaemia-reperfusion injury.
Document type:: Journal Article; Article
Author(s):: Moritz, Martina; Pfeifer, Sabine; Balmayor, Elizabeth R; Mittermayr, Rainer; Wolbank, Susanne; Redl, Heinz; Van Griensven, Martijn
Abstract:: Skeletal ischaemia-reperfusion (I-R) injury may influence patient outcome after severe vascular trauma or clamping of major vessels. The aim of this study was to observe whether locally applied vascular endothelial growth factor (VEGF) in fibrin could induce the expression of VEGF-receptor-2 (VEGFR-2) and improve the outcome after I-R injury. Transgenic mice expressing VEGFR-2 promoter-controlled luciferase were used for the assessment of VEGFR-2 expression. Ischaemia was induced for 2 h by a tension-controlled tourniquet to the hind limb, followed by 24 h of reperfusion. The animals were locally injected subcutaneously with fibrin sealant containing 20 or 200 ng VEGF; control animals received no treatment or fibrin sealant application. In vivo VEGFR-2 expression was quantified upon administration of luciferin at several observation times. For oedema and inflammation quantification, wet:dry ratio measurements and a myeloperoxidase assay of the muscle tissue were performed. Laser Doppler imaging showed that ischaemia was present and that the blood flow had returned to baseline levels after 24 h of reperfusion. VEGFR-2 expression levels in the fibrin + 200 ng VEGF were significantly higher than in all other groups. Granulocyte infiltration was reduced in both treatment groups, as well as reduced oedema formation. These results showed that VEGF released from fibrin had a positive effect on early I-R outcome in a mouse model, possibly via VEGFR-2. Copyright © 2016 John Wiley & Sons, Ltd.
Journal title abbreviation:: J Tissue Eng Regen Med
Year:: 2017
Journal volume:: 11
Journal issue:: 7
Pages contribution:: 2153-2163
Fulltext / DOI:: doi:10.1002/term.2114
Pubmed ID:: http://view.ncbi.nlm.nih.gov/pubmed/26777435
Print-ISSN:: 1932-6254
TUM Institution:: Klinik und Poliklinik für Unfallchirurgie
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mediaTUM Gesamtbestand Einrichtungen Schools TUM School of Medicine and Health Departments Clinical Medicine Klinik und Poliklinik für Unfallchirurgie (Prof. Biberthaler)2017