Role of Inhibitory Transforming Growth Factor-β Signal Smad7 in Helicobacter pylori-associated Gastric Damage.
10.4166/kjg.2016.68.4.186
- Author:
Ho Jae LEE
1
;
Jong Min PARK
;
Ki Baik HAHM
Author Information
1. Department of Biochemistry, Gachon University School of Medicine, Incheon, Korea.
- Publication Type:Original Article
- Keywords:
Helicobacter pylori;
Transforming growth factor beta;
Smad7;
Gastritis
- MeSH:
Apoptosis;
Cyclooxygenase 2;
Gastritis;
Gastrointestinal Neoplasms;
Helicobacter pylori;
Helicobacter*;
Heme Oxygenase-1;
Inflammation;
Neoplasm Metastasis;
Nitric Oxide Synthase;
RNA, Small Interfering;
Transforming Growth Factor beta
- From:The Korean Journal of Gastroenterology
2016;68(4):186-194
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: Transforming growth factor-beta (TGF-β) is a cytokine implicated in the susceptibility, development, and progression of gastrointestinal cancer and certain other neoplasms. In the later stages of cancer, TGF-β not only acts as a bystander of host-immune response, but also contributes to cell growth, invasion, and metastasis. In the current study, we generated gastric mucosal cells that stably express Smad7, and explored the Helicobacter pylori-associated biological changes between mock-transfected and Smad7-transfected RGM1 cells. METHODS: RGM1 cells stably transfected with Smad7 were infected with H. pylori, and molecular changes in apoptotic markers and inflammatory mediators were examined. Several candidate genes were explored in Smad7-overexpressing cells after H. pylori infection. RESULTS: Overexpression of Smad7 in RGM1 cells significantly increased the H. pylori-induced cytotoxicity compared to mock-transfected cells. Exaggerated increases in inflammatory mediators, cyclooxygenase 2, inducible NO synthase, and augmented apoptosis were noted in Smad7-overexpressing cells, whereas mitigated heme oxygenase 1 was noted in Smad7- overexpressing cells. These phenomena were reversed in cells transfected with Smad7 siRNA. CONCLUSIONS: These data suggest that inhibition of Smad7 is a possible target for mitigating H. pylori-associated inflammation.
