Pancreatic metaplasia in the gastro-achlorhydria in WTC-dfk rat, a potassium channel Kcnq1 mutant
Pancreatic metaplasia in the gastro-achlorhydria in WTC-dfk rat, a potassium channel Kcnq1 mutant
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DOI：
10.1354/vp.45-4-586
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发表时间：
2008-07-01
影响因子：
2.4
通讯作者：
Serikawa, T.
中科院分区：
文献类型：
--
作者：
Kuwamura, M.;Okajima, R.;Serikawa, T.
WTC耳聋京都（dfk）大鼠是一种新的突变体，其特征是耳聋和异常、不平衡的行为。 WTC-dfk 大鼠的 Kcnq1 基因存在基因内缺失； KCNQ1在K+稳态中发挥重要作用，Kcnq1的突变会导致人类心脏长QT综合征。在这里，我们研究了这些 WTC-dfk 大鼠的胃部病变。胃最典型的病理特征是胃体出现肥大的胃腺。肥大细胞胞浆内有较多嗜酸性颗粒，阿赞染色呈红色；胰蛋白酶原、淀粉酶和胰凝乳蛋白酶染色呈阳性；当使用免疫组织化学分析时，胃蛋白酶原染色未呈阳性。这些染色结果表明向胰腺腺泡细胞化生。 34周龄WTC-dfk大鼠的粘膜底部发现广泛的纤维化，表明胃部病变随着年龄的增长而进展。尽管WTC对照大鼠中增殖细胞核抗原阳性细胞仅限于腺颈区域，但WTC-dfk大鼠中的阳性细胞分散在整个粘膜中。 WTC-dfk 大鼠的壁细胞 KCNQ1 免疫组织化学分析呈阴性。这些发现表明，大鼠 Kcnq1 的缺陷会引起胃腺细胞的异常增殖和分化。
The WTC-deafness Kyoto (dfk) rat is a new mutant characterized by deafness and abnormal, imbalanced behavior. WTC-dfk rats carry an intragenic deletion at the Kcnq1 gene; KCNQ1 plays an important role in K+ homeostasis, and the mutation of Kcnq1 causes a cardiac long QT syndrome in humans. Here, we studied stomach lesions in these WTC-dfk rats. The most characteristic pathologic feature in the stomach was the appearance of hypertrophic gastric glands in the stomach body. The hypertrophic cells had many eosinophilic granules in their cytoplasm, and these granules were stained red with Azan stain; stained positively for trypsinogen, amylase, and chymotrypsin; and did not stain positively for pepsinogen when using immunohistochemical analysis. These staining results suggested a metaplasia toward a pancreatic acinar cells. Extensive fibrosis was found in the bottom part of the mucosa of 34-week-old WTC-dfk rats, suggesting a progression of stomach lesions with aging. Although cells that were positive for proliferating cell nuclear antigen were restricted in the area of the glandular neck in WTC control rats, positive cells in WTC-dfk rats were scattered throughout the mucosa. The parietal cells in WTC-dfk rats were negative for KCNQ1 immunohistochemical analysis. These findings indicate that a deficiency in rat Kcnq1 provokes an abnormal proliferation and differentiation of gastric glandular cells.