Role of FGF10/FGFR2b Signaling in Mouse Digestive Tract Development, Repair and Regeneration Following Injury

摘要: During embryonic development, the rudimentary digestive tract is initially a tube-like structure. It composed of epithelial cells surrounded by mesenchymal cells. Reciprocal epithelial-mesenchymal interactions progressively subdivide this primitive tube into distinct functional regions: tongue, pharynx, esophagus, stomach, duodenum, small intestine, cecum, large colon, and anus as well pancreas liver. Fibroblast growth factors (Fgfs) constitute family conserved proteins playing crucial roles during organogenesis, homeostasis, repair after injury. Among them, fibroblast factor 10 (Fgf10) has been reported to orchestrate development. In mice, loss function Fgf10 its receptor 2b (Fgfr2b) lead defective taste papillae in underdeveloped differentiation duodenal, cecal, colonic atresias, anorectal malformation, Fgf signaling through Fgfr2b also critical for process gut adult malabsorption disorder called bowel syndrome triggered massive resection (SBR). wild-type SBR leads regenerative adaptation characterized an increase diameter remaining intestine presence deeper crypts longer villi, altogether leading increased intestinal surface. Intestinal stem are key regeneration process. Induction expression Paneth located crypt following suggests role adaptation.