The role of vasculogenesis in the pathogenesis of intestinal atresia

摘要: Abstract Introduction: Invalidation of the Fibroblast growth factor 10 (Fgf10) pathway results in colonic atresia. Fetal liver kinase (Flk-1), a receptor for vascular endothelial factor, is critical vasculogenesis. The goal current study to evaluate role vasculogenesis (via Flk-1 expression), as pathogenic atresia caused by deletion Fgf10. Methods: Fgf10−/−, Fgf10nlacZ/+ & Flk-1nlacZ/+ mutant mouse strains were crossed, creating embryos with expressing lacZ reporter gene under control promoter Flk-1, Fgf10 or both. Photographs taken colon at developmental stages E10.5 - E18.5 after treatment X-Gal. Results: expressed and mesenteric vasculature end organ capillaries. Fgf10−/− demonstrate normal vasculature. capillaries tissue express time points relevant pathogenesis This pattern similar that wild type colon. Conclusions: data demonstrates expression colon, developing intestine. staining capillary network atretic indicates there no direct down regulation mutant. Contrary accepted theories intestinal atresia, not due failure development.