Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia

Takaharu Taketomi, Daigo Yoshiga, Koji Taniguchi, Takashi Kobayashi, Atsushi Nonami, Reiko Kato, Mika Sasaki, Atsuo Sasaki, Hitoshi Ishibashi, Maiko Moriyama, Kei Ichiro Nakamura, Junji Nishimura, Akihiko Yoshimura

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102 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)855-857
Number of pages3
JournalNature Neuroscience
Volume8
Issue number7
DOIs
Publication statusPublished - 2005 Jul 25
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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  • Cite this

    Taketomi, T., Yoshiga, D., Taniguchi, K., Kobayashi, T., Nonami, A., Kato, R., Sasaki, M., Sasaki, A., Ishibashi, H., Moriyama, M., Nakamura, K. I., Nishimura, J., & Yoshimura, A. (2005). Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia. Nature Neuroscience, 8(7), 855-857. https://doi.org/10.1038/nn1485