Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia
Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia
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DOI：
10.1038/nn1485
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发表时间：
2005-07-01
影响因子：
25
通讯作者：
Yoshimura, A
中科院分区：
文献类型：
--
作者：
Taketomi, T;Yoshiga, D;Yoshimura, A
我们在此报道，小鼠 Sprouty2 基因（也称为 Spry2）的缺失导致肠神经增生，从而导致食管贲门失弛缓症和假性肠梗阻。胶质细胞源性神经营养因子 (GDNF) 诱导肠神经细胞中 ERK 和 Akt 过度激活。抗 GDNF 抗体的施用可纠正 Sprouty2 缺陷小鼠的神经增生。我们发现 Sprouty2 是 GDNF 对新生儿发育或肠神经细胞存活的负调节因子。
We report here that loss of the Sprouty2 gene (also known as Spry2) in mice resulted in enteric nerve hyperplasia, which led to esophageal achalasia and intestinal pseudo-obstruction. Glial cell line-derived neurotrophic factor (GDNF) induced hyperactivation of ERK and Akt in enteric nerve cells. Anti-GDNF antibody administration corrected nerve hyperplasia in Sprouty2-deficient mice. We show Sprouty2 to be a negative regulator of GDNF for the neonatal development or survival of enteric nerve cells.