| Project/Area Number |
25860644
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Okayama University |
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Principal Investigator |
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| Research Collaborator |
MIYAHARA Nobuaki 岡山大学, 大学院保健学研究科, 教授 (70335610)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | RAGE / COPD |
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| Outline of Final Research Achievements |
Pulmonary emphysema is characterized by persistent inflammation and progressive alveolar destruction. The receptor for advanced glycation end-products (RAGE) is a multiligand cell surface receptor reported to be involved in the process of acute alveolar epithelial cell injury. RAGE-sufficient (RAGE(+/+)) mice and RAGE-deficient (RAGE(-/-)) mice were treated with intratracheal elastase. Neutrophilia in bronchoalveolar lavage fluid was reduced in elastase-treated RAGE(-/-) mice on Day 4, and was associated with decreased levels of some kind of cytokines. Static lung compliance values and emphysematous changes in the lung tissue were decreased in RAGE(-/-) mice on Day 21. Experiments using irradiated, bone marrow-chimeric mice identify the importance of RAGE expressed on lung structural cells in the development of elastase-induced pulmonary inflammation and emphysema. Thus, RAGE represents a novel therapeutic target for preventing pulmonary emphysema.
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