| Project/Area Number |
26860267
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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 |
Experimental pathology
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| Research Institution | Kinki University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 細胞間接着分子 / 細胞死 / 間質性肺炎 / 糖尿病 / プロテアーゼ / 耐糖能 / 炎症 |
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| Outline of Final Research Achievements |
Cell adhesion molecule 1 (CADM1) is expressed by lung alveolar cells and pancreatic islet cells, and is enzymatically shed at its juxtamembranous ectodomain. In the present study, we examined CADM1 expression in the lung of idiopathic interstitial pneumonia (IIP) and in the pancreata of type 2 diabetes mellitus (T2DM), and found that CADM1 ectodomain shedding increased in both cases. In IIP lungs, the increase of CADM1 shedding resulted in the decrease of full length CADM1 and led alveolar epithelical cell apoptosis, which assumed to be an early pathogenic event in the development of IIP. In T2DM, the CADM1 shedding rates and haemoglobin A1c levels were correlated, suggesting that increased CADM1 shedding in pancreata contributed to blood glucose dysregulation. Interestingly, in those disease, an imbalanced protease activity has been reported. Our studies lead us to identify the protease-mediated shedding of adhesion molecule as an important pathogenic process for tissue degeneration.
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