Mice lacking neurofibromin develop gastric hyperplasia

Lu Lin, Jian Chen, James A. Richardson, Luis F. Parada

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

Gastrointestinal (GI) neoplasms are among many manifestations of the genetic disease neurofibromatosis type 1 (NF1). However, the physiological and pathological functions of the Nf1 gene in the GI system have not been fully studied, possibly because of a lack of mouse models. In this study, we generated conditional knockout mice with Nf1 deficiency in the GI tract. These mice develop gastric epithelial hyperplasia and inflammation together with increased cell proliferation and apoptosis. The gastric phenotypes observed in these mutant mice seem to be the consequence of loss of Nf1 in gastric fibroblasts, resulting in paracrine hyperactivation of the ERK pathway in the gastric epithelium. These mice provide a useful model to study the pathogenesis of GI lesions in a subset of patients with NF1 and to investigate the role of the Nf1 gene in the development of GI neoplasms.

Original languageEnglish (US)
Pages (from-to)G751-G761
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume297
Issue number4
DOIs
StatePublished - 2009

Keywords

  • Islet1-Cre

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

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