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Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
Published on: May 7, 2018
Expression of cyclooxygenase-2 in human hyperplastic gastric polyps
1First Dept. of Internal Medicine, Saitama Medical Center, Saitama Medical School, Kamoda Kawagoe, Saitama, Japan. bam@saitama-med.ac.jp
Journal of Experimental & Clinical Cancer Research : CR
|October 30, 2003
Summary
Helicobacter pylori infection induces cyclooxygenase (COX)-2 in gastric polyps. This COX-2 expression in mesenchymal cells may contribute to polyp development, suggesting a target for intervention.
Area of Science:
- Gastroenterology
- Oncology
- Immunology
Background:
- Cyclooxygenase (COX)-2 is a target for colon cancer prevention by NSAIDs.
- Helicobacter pylori (H. pylori) infection can induce COX-2 and inflammatory cytokines.
- The role of COX-2 in H. pylori-associated gastric polyp regression is unclear.
Purpose of the Study:
- To investigate COX-2 expression and localization in human hyperplastic gastric polyps.
- To determine the cellular sources of COX-2 in these polyps.
Main Methods:
- Immunohistochemistry was used to examine COX-2 expression in 12 gastric polyp specimens.
- Antibodies against COX-2, CD68 (macrophages), and alpha-smooth muscle actin (myofibroblasts) were utilized.
- Formalin-fixed, paraffin-embedded tissues were analyzed using an avidin-biotin complex method.
Main Results:
- Strong COX-2 immunoreactivity was predominantly observed in sub-epithelial interstitial cells of 10 polyps.
- A significant increase in interstitial COX-2 expression was found.
- COX-2 staining partially overlapped with macrophages and myofibroblasts.
Conclusions:
- H. pylori-induced COX-2 in mesenchymal cells may play a role in gastric hyperplastic polyp tumorigenesis.
- Targeting COX-2 in mesenchymal cells could be a strategy for managing H. pylori-related gastric polyps.
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