Search for drug seeds for treatment of pulmonary emphysema targeting adhesion molecules

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19079
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Experimental pathology
• Research Institution: Kindai University
• Principal Investigator: HAGIYAMA Mitsuru 近畿大学, 医学部, 助教 (60632718)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: アポトーシス / 接着分子 / shedding

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.

Free Research Field

実験病理