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

被引：113

作者：

Taketomi, T

Yoshiga, D

Taniguchi, K

Kobayashi, T

Nonami, A

Kato, R

Sasaki, M

Sasaki, A

Ishibashi, H

Moriyama, M

Nakamura, K

Nishimura, J

Yoshimura, A

机构：

[1] Kyushu Univ, Med Inst Bioregulat, Div Mol & Cellular Immunol, Higashi Ku, Fukuoka 8128582, Japan

[2] Kyushu Univ, Fac Dent Sci, Div Oral & Maxillofacial Oncol, Higashi Ku, Fukuoka 8128582, Japan

[3] Kyushu Univ, Fac Med, Dept Physiol, Higashi Ku, Fukuoka 8128582, Japan

[4] Kurume Univ, Sch Med, Dept Anat, Kurume, Fukuoka 8300011, Japan

[5] Kyushu Univ, Grad Sch Med Sci, Res Inst Angiocardiol, Div Mol Cardiol, Fukuoka 8128582, Japan

来源：

NATURE NEUROSCIENCE | 2005年 / 8卷 / 07期

关键词：

D O I：

10.1038/nn1485

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

收藏

页码：855 / 857

页数：3

相关论文

共 11 条

[1] Enteric nervous system progenitors are coordinately controlled by the G protein-coupled receptor EDNRB and the receptor tyrosine kinase RET [J].

Barlow, A ;

de Graaff, E ;

Pachnis, V .

NEURON, 2003, 40 (05) :905-916

[2] Sprouty1 is a critical regulator of GDNF/RET-mediated kidney induction [J].

Basson, MA ;

Akbulut, S ;

Watson-Johnson, J ;

Simon, R ;

Carroll, TJ ;

Shakya, R ;

Gross, I ;

Martin, GR ;

Lufkin, T ;

McMahon, AP ;

Wilson, PD ;

Costantini, FD ;

Mason, IJ ;

Licht, JD .

DEVELOPMENTAL CELL, 2005, 8 (02) :229-239

[3]

GHOSH P, 1994, AM J GASTROENTEROL, V89, P1880

[4] A MUTATION IN THE RET PROTOONCOGENE ASSOCIATED WITH MULTIPLE ENDOCRINE NEOPLASIA TYPE-2B AND SPORADIC MEDULLARY-THYROID CARCINOMA [J].

HOFSTRA, RMW ;

LANDSVATER, RM ;

CECCHERINI, I ;

STULP, RP ;

STELWAGEN, T ;

LUO, Y ;

PASINI, B ;

HOPPENER, JWM ;

VANAMSTEL, HKP ;

ROMEO, G ;

LIPS, CJM ;

BUYS, CHCM .

NATURE, 1994, 367 (6461) :375-376

[5] The mechanism for the contraction induced by leukotriene C4 in guinea-pig taenia coil [J].

Ieiri, S ;

Nishimura, J ;

Hirano, K ;

Suita, S ;

Kanaide, H .

BRITISH JOURNAL OF PHARMACOLOGY, 2001, 133 (04) :529-538

[6] GDNF-induced activation of the Ret protein tyrosine kinase is mediated by GDNFR-alpha, a novel receptor for GDNF [J].

Jing, SQ ;

Wen, DZ ;

Yu, YB ;

Holst, PL ;

Luo, Y ;

Fang, M ;

Tamir, R ;

Antonio, L ;

Hu, Z ;

Cupples, R ;

Louis, JC ;

Hu, S ;

Altrock, BW ;

Fox, GM .

CELL, 1996, 85 (07) :1113-1124

[7] Modulation of signalling by sprouty: A developing story [J].

Kim, HJ ;

Bar-Sagi, D .

NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2004, 5 (06) :441-450

[8] CLINICAL AND HISTOLOGIC-STUDIES OF NEURONAL INTESTINAL DYSPLASIA [J].

MUNAKATA, K ;

MORITA, K ;

OKABE, I ;

SUEOKA, H .

JOURNAL OF PEDIATRIC SURGERY, 1985, 20 (03) :231-235

[9] ACTIVATION OF RET AS A DOMINANT TRANSFORMING GENE BY GERMLINE MUTATIONS OF MEN2A AND MEN2B [J].

SANTORO, M ;

CARLOMAGNO, F ;

ROMANO, A ;

BOTTARO, DP ;

DATHAN, NA ;

GRIECO, M ;

FUSCO, A ;

VECCHIO, G ;

MATOSKOVA, B ;

KRAUS, MH ;

DIFIORE, PP .

SCIENCE, 1995, 267 (5196) :381-383

[10] Sprouty2, a mouse deafness gene, regulates cell fate decisions in the auditory sensory epithelium by antagonizing FGF signaling [J].

Shim, K ;

Minowada, G ;

Coling, DE ;

Martin, GR .

DEVELOPMENTAL CELL, 2005, 8 (04) :553-564