Differentiation of the Gastric Mucosa III. Animal models of oxyntic atrophy and metaplasia

被引：68

作者：

Goldenring, James R.

Nomura, Sachiyo

机构：

[1] Vanderbilt Univ, Sch Med, Dept Surg, Epithelial Biol Program, Nashville, TN 37232 USA

[2] Vanderbilt Univ, Sch Med, Dept Cell & Dev Biol, Nashville, TN 37232 USA

[3] Vanderbilt Univ, Sch Med, Nashville Dept Vet Affairs Med Ctr, Nashville, TN 37232 USA

[4] Univ Tokyo, Grad Sch Med, Dept Gastrointestinal Surg, Tokyo 106, Japan

来源：

AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 2006年 / 291卷 / 06期

关键词：

gastric adenocarcinoma; spasmolytic polypeptide expressing metaplasia; trefoil factor 2; intestinal metaplasia;

D O I：

10.1152/ajpgi.00187.2006

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Gastric cancer in humans arises in the setting of oxyntic atrophy (parietal cell loss) and attendant hyperplastic and metaplastic lineage changes within the gastric mucosa. Helicobacter infection in mice and humans leads to spasmolytic polypeptide-expressing metaplasia (SPEM). In a number of mouse models, SPEM arises after oxyntic atrophy. In mice treated with the parietal cell toxic protonophore DMP-777, SPEM appears to arise from the transdifferentiation of chief cells. These results support the concept that intrinsic mucosal influences regulate and modulate the appearance of gastric metaplasia even in the absence of significant inflammation, whereas chronic inflammation is required for the further neoplastic transition.

引用

页码：G999 / G1004

页数：6

共 26 条

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