| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Research Abstract |
Cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD), but the mechanisms of pathogenesis are incompletely defined. We have previously reported that senescence marker protein-30 knockout (SMP30-KO) mice can be useful for investigating cigarette smoke-induced pulmonary emphysema. Moreover, we have already shown that miR-146a plays a pathogenetic role in the abnormal inflammatory response in COPD.
Vitamin C-controlled SMP30-KO were given miR-146a inhibitor on day 1 and 8 intranasally during exposure to either diluted cigarette smoke or fresh air for 2 weeks. Total cell and lymphocyte numbers were increased in the BALF of both miR-146a inhibitor and smoke exposed mice. PGE2 production and COX-2 expression were also increased significantly higher by exposure both miR-146a inhibitor and cigarette smoke.
In conclusion, miR-146a appears to play a pathogenetic role in the abnormal inflammatory response in a cigarette smoke-exposed murine model of COPD.
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