Endoplasmic reticulum stress is involved in H. Pylori associated gastritis
Project/Area Number |
22890138
|
Research Category |
Grant-in-Aid for Research Activity Start-up
|
Allocation Type | Single-year Grants |
Research Field |
Gastroenterology
|
Research Institution | Nagasaki University |
Principal Investigator |
|
Project Period (FY) |
2010 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥2,834,000 (Direct Cost: ¥2,180,000、Indirect Cost: ¥654,000)
Fiscal Year 2011: ¥1,469,000 (Direct Cost: ¥1,130,000、Indirect Cost: ¥339,000)
Fiscal Year 2010: ¥1,365,000 (Direct Cost: ¥1,050,000、Indirect Cost: ¥315,000)
|
Keywords | VacA / ヘリコバクターピロリ / BH3オンリー蛋白 / アポトーシス / ER stress / ヘリコバクター・ピロリ |
Research Abstract |
Apoptosis by H. pylori vactuolating cytotoxin(VacA) plays a role in H. Pylori induced apoptosis in gastric epitherial cells. However, precise mechanism of VacA apoptosis is not understood. Our aim was to examine involvement of ER stress and pro-apoptotic BH3 only proteins in human H. Pylori infection and in VacA treated cells. GADD34 mRNA and GRP 78 mRNA were significantly increased in H. Pylori infected gastric mucosa. Immunohistochemistry showed CRP78 staining in gastric epitherial cells. Apoptosis inducing ER stress marker CHOP was significantly elevated in AZ521 treated with VacA, and was contributing to apoptosis. The present study is, to our knowledge, among the first to implicate the association of ER stress with human H. Pylori infection and its apoptosis inducing toxin, VacA.
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Report
(3 results)
Research Products
(8 results)