Differentiation of the Gastric Mucosa III. Animal models of oxyntic atrophy and metaplasia
Differentiation of the Gastric Mucosa III. Animal models of oxyntic atrophy and metaplasia
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DOI：
10.1152/ajpgi.00187.2006
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发表时间：
2006-12-01
影响因子：
4.5
通讯作者：
Nomura, Sachiyo
中科院分区：
文献类型：
--
作者：
Goldenring, James R.;Nomura, Sachiyo
人类的胃癌发生在胃黏膜内氧合萎缩(壁细胞丢失)和伴随的增生性和化生性谱系改变的背景下。小鼠和人的幽门螺杆菌感染导致痉挛多肽表达化生(SPEM)。在许多小鼠模型中，SPEM是在氧合萎缩后出现的。在用壁细胞毒性原载体DMP-777治疗的小鼠中，SPEM似乎是由主细胞的转分化而产生的。这些结果支持这样的观点，即即使在没有明显炎症的情况下，内在的粘膜影响也调节和调节胃化生的出现，而进一步的肿瘤转移需要慢性炎症。
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.