Cellular proliferation and differentiation in rat atrophic gastric mucosa induced by N'-methyl-N'-nitro-N-nitrosoguanidine

J Clin Gastroenterol. 1997:25 Suppl 1:S116-21. doi: 10.1097/00004836-199700001-00020.

Abstract

It has been demonstrated that mucosal cell proliferation in atrophic gastritis is significantly accelerated, although the dynamics of the cell proliferation and differentiation have not been well characterized. We sequentially analyzed the markers of proliferation and differentiation of rat atrophic gastritis induced by MNNG. Immunohistochemical staining by anti-BrdU, anti-PCNA, and anti-PDGF-BB antibodies demonstrated that cell proliferation in atrophic gastritis was accelerated not only in the parenchymal tissue but also in the mesenchymal tissue. Expression of a gap junction protein (connexin 32), which is a marker for differentiation of epithelial cells, was reduced during the progression of atrophy. Some apoptotic cells were observed in the lower to middle third of the atrophic mucosa, whereas apoptotic cells were rarely seen in normal mucosa, which suggests that apoptosis in these parts of the mucosa may be related to the occurrence of mucosal atrophy.

MeSH terms

  • Animals
  • Apoptosis
  • Cell Differentiation / drug effects
  • Cell Division / drug effects
  • Connexins / biosynthesis
  • Gap Junction beta-1 Protein
  • Gastric Mucosa / drug effects
  • Gastric Mucosa / pathology
  • Gastritis, Atrophic / chemically induced*
  • Gastritis, Atrophic / pathology*
  • Male
  • Methylnitronitrosoguanidine*
  • Rats
  • Rats, Wistar

Substances

  • Connexins
  • Methylnitronitrosoguanidine