2017 Fiscal Year Final Research Report
Induction of cardiovascular lesions by Helicobacter pylori
| Project/Area Number |
16K15273
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Bacteriology (including mycology)
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Keywords | 毒素・エフェクター / ピロリ菌 / CagA / エクソソーム |
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| Outline of Final Research Achievements |
Recent epidemiological studies suggest the relationship between cardiovascular diseases such as angina pectoris and myocardial infarction and chronic infection with H. pylori producing the oncogenic effector protein CagA. Following injection into gastric epithelial cells, a fraction of CagA proteins are incorporated into exosomes, which are secreted from the epithelial cells into the general circulation. This suggests that CagA reaches vascular endothelial cells via exosomes. We found in this work that, in vascular endothelial cells, CagA induces EMT-like morphological transformation and elevated cell motility in its tyrosine phosphorylation-dependent manner. We also succeeded in establishing genetically engineered mice that specifically express CagA in vascular endothelial cells or gastrointestinal cells, which provide an excellent in vivo model system in investigating the role of H. pylori CagA in cardiovascular lesions.
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| Free Research Field |
感染腫瘍学、分子腫瘍学
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