Role of Inhibitory Transforming Growth Factor-β Signal Smad7 in Helicobacter pylori-associated Gastric Damage헬리코박터 파일로리 감염 연관 위질환 발생시 형질전환인자-베타 저해신호로서 Smad7의 역할
- Other Titles
- 헬리코박터 파일로리 감염 연관 위질환 발생시 형질전환인자-베타 저해신호로서 Smad7의 역할
- Authors
- 이호재; 박종민; 함기백
- Issue Date
- Oct-2016
- Publisher
- 대한소화기학회
- Keywords
- Helicobacter pylori; Transforming growth factor beta; Smad7; Gastritis
- Citation
- 대한소화기학회지, v.68, no.4, pp.186 - 194
- Journal Title
- 대한소화기학회지
- Volume
- 68
- Number
- 4
- Start Page
- 186
- End Page
- 194
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/9116
- DOI
- 10.4166/kjg.2016.68.4.186
- ISSN
- 1598-9992
- Abstract
- Background/Aims: Transforming growth factor-beta (TGF-) is a cytokine implicated in the susceptibility, development, and progression of gastrointestinal cancer and certain other neoplasms. In the later stages of cancer, TGF- 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.
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