Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia
T Taketomi, D Yoshiga, K Taniguchi, T Kobayashi… - Nature …, 2005 - nature.com
Nature neuroscience, 2005•nature.com
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.
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.
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.
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