Journal of pediatric surgery · 2003
Analysis of the effects of endothelin-3 on the development of neural crest cells in the embryonic mouse gut.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Woodward Mark N, Sidebotham Emma L, Connell M Gwen, Kenny Simon E, Vaillant Camille R, Lloyd David A, Edgar David H
Аннотация
BACKGROUND/PURPOSE: Mutations in the endothelin-3 (ET-3) and endothelin-B receptor (EDNR-B) genes cause terminal colonic aganglionosis in mice and are linked to Hirschsprung's disease. These experiments are designed to determine if the development of terminal enteric ganglia depends on changes in proliferation, apoptosis, or differentiation of enteric neural crest (NC) cells in response to ET-3.
METHODS: Gut from embryonic lethal-spotted mice (lacking ET-3) and controls were investigated in vivo. NC-derived cells were identified immunohistochemically and their proliferation, apoptosis and differentiation monitored by bromodeoxyuridine incorporation, the terminal deoxytransferase poly dU nick end labelling (TUNEL) reaction, and appearance of neuronal nitric oxide synthase (NOS), respectively.
RESULTS: No differences in apoptosis or proliferation of NC cells were apparent between lethal-spotted embryos and controls. Although no temporal differences in the differentiation of NOS neurones were evident, these cells appeared more cranially in the gut in the absence of ET-3 than in controls.
CONCLUSIONS: ET-3 has no detectable influence on proliferation, apoptosis, or timing of differentiation of NC-derived cells in the gut. However, the more proximal location of differentiated neurones in the absence of ET-3 is consistent with a restricted role in migration of NC-derived cells.
METHODS: Gut from embryonic lethal-spotted mice (lacking ET-3) and controls were investigated in vivo. NC-derived cells were identified immunohistochemically and their proliferation, apoptosis and differentiation monitored by bromodeoxyuridine incorporation, the terminal deoxytransferase poly dU nick end labelling (TUNEL) reaction, and appearance of neuronal nitric oxide synthase (NOS), respectively.
RESULTS: No differences in apoptosis or proliferation of NC cells were apparent between lethal-spotted embryos and controls. Although no temporal differences in the differentiation of NOS neurones were evident, these cells appeared more cranially in the gut in the absence of ET-3 than in controls.
CONCLUSIONS: ET-3 has no detectable influence on proliferation, apoptosis, or timing of differentiation of NC-derived cells in the gut. However, the more proximal location of differentiated neurones in the absence of ET-3 is consistent with a restricted role in migration of NC-derived cells.