Search for drug seeds for treatment of pulmonary emphysema targeting adhesion molecules
Project/Area Number |
15K19079
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Experimental pathology
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Research Institution | Kindai University |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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Keywords | アポトーシス / 接着分子 / shedding / 肺気腫 |
Outline of Final Research Achievements |
Pulmonary emphysema arises in cigarette smokers and also ex-smokers, indicating that alveolar structural destruction progresses even in the absence of oxidants. Lung-epithelial cell adhesion molecule 1 (CADM1) is extracellularly shed. This event contributes to the development of emphysema through accumulating the proapoptotic shedding products within alveolar cells. Here, we made an ex-smoker model using C57BL/6 mice. We calculated the mean linear intercepts in the lung histologic sections to estimate the alveolar space dilatation. The alveolar airspace was unchanged at the age of 18 weeks, but was significantly dilated at 30 weeks when compared with age-matched mice (p=0.016). Western blot analyses of the lung lysates revealed that the mice of both ages had more CADM1 shedding products than age-matched mice (p<0.05). Persisting increase in ectodomain shedding of CADM1 appeared to contribute to the development of emphysema in ex-smokers.
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Report
(3 results)
Research Products
(9 results)
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[Journal Article] The intracellular domain of cell adhesion molecule 1 is present in emphysematous lungs and induces lung epithelial cell apoptosis.2015
Author(s)
1.Hagiyama, M., Yoneshige, A., Inoue, T., Sato, Y., Mimae, T., Okada, M., Ito, A.
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Journal Title
J. Biomed. Sci
Volume: 22
Issue: 1
Pages: 67-67
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Increased ectodomain shedding of cell adhesion molecule 1 as a cause of type II alveolar epithelial cell apoptosis in patients with idiopathic interstitial pneumonia.2015
Author(s)
2.Yoneshige, A., Hagiyama, M., Inoue, T., Mimae, T., Kato, T., Okada, M., Enoki, E., Ito, A.
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Journal Title
Respir. Res.
Volume: 16
Issue: 1
Pages: 90-90
DOI
Related Report
Peer Reviewed / Open Access
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