哺乳动物Sprouty2缺失会导致肠道神经元增生和食管失弛缓症。
Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia.
作者信息
Taketomi Takaharu, Yoshiga Daigo, Taniguchi Koji, Kobayashi Takashi, Nonami Atsushi, Kato Reiko, Sasaki Mika, Sasaki Atsuo, Ishibashi Hitoshi, Moriyama Maiko, Nakamura Kei-ichiro, Nishimura Junji, Yoshimura Akihiko
机构信息
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
出版信息
Nat Neurosci. 2005 Jul;8(7):855-7. doi: 10.1038/nn1485.
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.
我们在此报告，小鼠中Sprouty2基因（也称为Spry2）缺失导致肠神经增生，进而引发食管失弛缓症和肠道假性梗阻。胶质细胞系衍生的神经营养因子（GDNF）诱导肠神经细胞中ERK和Akt过度激活。给予抗GDNF抗体可纠正Sprouty2缺陷小鼠的神经增生。我们证明Sprouty2是肠神经细胞新生发育或存活过程中GDNF的负调节因子。
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