Expression profiling the developing mammalian enteric nervous system identifies marker and candidate Hirschsprung disease genes
 PNAS vol. 103. no. 18. P. 6919-6924 (2006) | |||
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Рисунки из статьи CHERYL E. GARIEPY . Pediatric Research 49:605-613.2001
) Рис.1. | Schematic presentation of the colonization of the developing gut by NC-derived cells. Vagal NC-derived cells (shown in red) migrate ventrally to populate the entire gut. Truncal NC-derived cells (shown in blue) populate the foregut. The foregut is, therefore, populated by both vagal and truncal NC-derived cells (shown in purple). Sacral NC-derived cells (shown in green) colonize the hindgut before the arrival of the vagal NC-derived cells. ) Рис.2. | Schematic presentation of the NC-derived cell contribution to the mammalian ENS. Truncal NC-derived cells (shown in blue) populate the esophagus and gastric cardia. These cells are able to colonize the gut in the absence of ret activation. However, survival of these cells appears to be dependent upon mash1 expression. Vagal NC-derived cells (shown in red/orange) populated the entire gut. These cells are unable to colonize the gut in the absence of ret activation and phox2b expression, likely due to the regulation of ret expression by phox2b. Development of a subset of these cells in the distal gut also appears to be dependent upon mash1 expression. Vagal NC-derived cells fail to completely colonize the hindgut in the absence of ednrb activation in the region of the cecum. The length of aganglionosis resulting from ednrb-deficiency ranges from total colonic to short distal segment, depending on unidentified modifying genes. Ncx appears to be important for postnatal apoptosis in the colonic ENS. In the absence of ncx, the ENS exhibits a physiologically important increased number of neurons. The final contribution to the ENS by sacral NC-derived cells is unclear, as the hindgut ENS fails to develop in the absence of hindgut colonization by the vagal NC-derived cells. |
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