Factor Xlll-deficient patients have impaired wound healing, but the mechanistic role of factor XIII in wound healing remains unclear. Our work shows the human microvascular endothelial cell line, HMEC-1, binds immobilized factor XIIla, but not iodoacetamide-inactivated factor XHIa, in a dose-dependent manner. Binding of soluble factor Xllla to HMEC-ls was confirmed by fluorescence activated cell sorting analysis. An antibody to β1 integrins blocked binding of HMEC-ls to factor Xllla 60%, while an antibody to avβz decreased binding 70%. and a combination of the antibodies reduced binding >95%. To examine the role of factor Xllla in wound repair, a three-dimensional microcarrier-based in vitro angiogenesis assay was conducted. Factor XIII was removed from γ A/γA and γA/γfibrinogen by urea treatment. HMEC- Is stimulated for angiogenesis with basic fibroblast growth factor or vascular endothelial growth factor in γA/-γA and γA/-γ fibrin clots showed decreased cell migration and sprout length in the presence of factor Xllla, however, the number of capillary-like sprouts per microcarrier remained unchanged. In conclusion, factor Xllla may play a role in wound repair by binding microvascular endothelial cells in an integrin dependent manner and affecting cell migration and sprout length during angiogenesis.
|Original language||English (US)|
|State||Published - Dec 1 1998|
ASJC Scopus subject areas
- Molecular Biology