Résumé :
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Hirschprung disease may be considered as an intestinal neuropathy with muscular dysfunction. Some hope for its treatment has appeared with cellular therapy. Aim: to test the possibility of intestinal nervous ganglia reconstruction . Material, methods: To study intestinal reconstruction features, syngenic fetal intestine implantation was provided in 30 Fischer rats (site: subcutaneous pouch of the ear pavilion). HE , connexin-43, nestin, vimentin and actin staining allowed evaluation of graft maturation state. Host cell participation in graft development, was evaluated by grafing fetal intestine of “wild type” mice C57Bl (WT) to 30 green fluorescent protein (b-actin-GFP) transgenic mice (same site). HE , GFP and SOX-10 staining were used to identify host cells in the graft and to detect neuronal precursors. Results. After initial graft ischaemic destruction, reconstruction and growth of the organ were observed. The reconstruction beginning corresponded to an increase of IGF-1 levels in the recipient serum, and of nestin and connexin-43 expression in the graft. Actin and vimentin were first absent and reappeared as smooth muscle differentiation started. After 1 month, muscular layers and myenteric plexuses were well-developed. In mice, GFP positive cells, coming only from the GFP host indeed, were identified in the implant, including muscular layers and many neurons. Conclusion. Remaining alive initially grafted cells, as well as host cell, incorporated in the graft, grew and differentiated into the different layers of intestine, including neuronal ganglia, according to ontogenic patterns. . Moreover the graft modifies host metabolism, as increased host serum IGF-1 level testimonies. . These observations opens potentialities for cellular therapy in Hirschprung disease
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