Development of Pancreatic Acinar Cell Metaplasia During Gastric Repair in a Rat Duodenal Contents Reflux Model.

Development of Pancreatic Acinar Cell Metaplasia During Gastric Repair in a Rat Duodenal Contents Reflux Model.
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DOI:
10.1007/s10620-020-06342-y
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发表时间:
2021-04
影响因子:
3.1
通讯作者:
Kushima R
Kushima R
中科院分区:
医学3区
文献类型:
--
作者:
Wada Y;Mukaisho KI;Kanai S;Nakayama T;Fukuda M;Mizukami K;Okimoto T;Kodama M;Sugihara H;Murakami K;Kushima R

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我们先前报道了十二指肠内容物反流模型(反流模型)在腺胃中发生胰腺腺泡细胞化生(PACM)。我们的目的是利用反流模型研究PACM的特征和组织发生。用8周大的雄性Wistar大鼠建立了反流模型,这些大鼠在术后30周内被处死。组织学检查分析腺胃-空肠吻合情况。此外,将PACM样本的电子显微镜图像与从未接受手术的大鼠的胰腺和胃腺切除的图像进行了比较。对α-淀粉酶、HIK1083、TFF2和Ki-67进行免疫组织化学染色,并用α-淀粉酶和HIK1083或α-淀粉酶和TFF2抗体进行双重荧光染色。在所有反流模型大鼠中,在腺胃-空肠吻合口近端可见PACM,周围可见假幽门化生。发生PACM的腺体深部主细胞减少。电子显微镜显示,PACM细胞的粗面内质网管数量多于主细胞,呈胰腺腺泡细胞形态。免疫组织化学染色显示,再生的黄斑上皮和部分假性幽门腺体呈TFF2强阳性,而PACM细胞仅呈弱阳性。α-淀粉酶和TFF2双阳性,而HIK1083阴性。十二指肠内容物反流可诱发PACM。PACM起源于胃粘膜再生过程中位于胃泌腺颈部的干细胞。
We previously reported the development of pancreatic acinar cell metaplasia (PACM) in the glandular stomach of a duodenal contents reflux model (reflux model). We aimed to investigate the characteristics and histogenesis of PACM using a reflux model. A reflux model was created using 8-week-old male Wistar rats, which were killed up to 30 weeks postoperatively. Histological examination was performed to analyze the glandular stomach–jejunal anastomosis. Furthermore, electron microscopic images of PACM samples were compared with pancreatic and gastric glands removed from rats that had not undergone surgery. Immunostaining for α-amylase, HIK1083, TFF2, and Ki-67 was performed, and double fluorescent staining was carried out using antibodies against α-amylase and HIK1083, or α-amylase and TFF2. In all reflux model rats, PACM was observed proximal to the glandular stomach–jejunal anastomosis, surrounded by pseudopyloric metaplasia. The number of chief cells was decreased in the deep part of the gland, where PACM occurred. Electron microscopy showed that PACM cells had greater numbers of rough endoplasmic reticulum tubules than chief cells, and exhibited pancreatic acinar cell morphology. Upon immunochemical staining, the regenerative foveolar epithelium and part of the pseudopyloric glands stained strongly positive for TFF2, whereas PACM cells were only weakly positive. Double fluorescent staining identified early lesions of PACM in the neck, which were double positive for α-amylase and TFF2, but negative for HIK1083. PACM could be induced by duodenal contents reflux. PACM originates from stem cells located in the neck of oxyntic glands during gastric mucosal regeneration.
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