Development of Pancreatic Acinar Cell Metaplasia During Gastric Repair in a Rat Duodenal Contents Reflux Model
Yasuhiro Wada1,2,3, Ken-Ichi Mukaisho4, Shunpei Kanai2
1Department of Gastroenterology, Faculty of Medicine, Oita University, Yufu, Oita, Japan.
Background:
We previously reported the development of pancreatic acinar cell metaplasia (PACM) in the glandular stomach of a duodenal contents reflux model (reflux model).
Aims:
We aimed to investigate the characteristics and histogenesis of PACM using a reflux model.
Methods:
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.
Results:
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.
Conclusions:
PACM could be induced by duodenal contents reflux. PACM originates from stem cells located in the neck of oxyntic glands during gastric mucosal regeneration.
Insights
Pancreatic acinar cell metaplasia (PACM) in the stomach is induced by duodenal reflux. This metaplasia originates from stem cells in the gastric oxyntic gland neck during regeneration.
Area of Science:
- Gastroenterology
- Cell Biology
- Regenerative Medicine
Background:
- Pancreatic acinar cell metaplasia (PACM) was previously observed in the glandular stomach of a duodenal contents reflux model.
- Understanding the characteristics and origin of PACM is crucial for gastrointestinal research.
Purpose of the Study:
- To investigate the characteristics and histogenesis of pancreatic acinar cell metaplasia (PACM).
- To utilize a duodenal contents reflux model in rats to study PACM development.
Main Methods:
- Created a reflux model in Wistar rats and observed them for up to 30 weeks.
- Performed histological, electron microscopic, and immunohistochemical analyses (α-amylase, HIK1083, TFF2, Ki-67).
- Utilized double fluorescent staining to identify early PACM lesions.
Main Results:
- PACM was consistently found proximal to the glandular stomach-jejunal anastomosis, near pseudopyloric metaplasia.
- Electron microscopy revealed PACM cells with abundant rough endoplasmic reticulum, resembling pancreatic acinar cells.
- Early PACM lesions in the neck of oxyntic glands were positive for α-amylase and TFF2.
Conclusions:
- Duodenal contents reflux can induce pancreatic acinar cell metaplasia (PACM) in the stomach.
- PACM arises from stem cells within the neck of oxyntic glands during gastric mucosal regeneration.
