| Project/Area Number |
12670580
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Tokyo Woman's Medical University |
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Principal Investigator |
AOSHINA Kazutetsu Tokyo Women's Medical University, School of Medicine, Assistant Professor, 医学部, 講師 (60231776)
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| Co-Investigator(Kenkyū-buntansha) |
安井 修司 東京女子医科大学, 医学部, 講師 (30147392)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | apoptpsis / pulmonary emphysema / chronic obstructive pulmonary disease / caspase / cell death / エラスターゼ / 肺胞上皮細胞 |
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| Research Abstract |
Pulmonary emphysema is characterized by destruction and loss of alveolar walls. Recent evidence indicates that epithelial or endothelial apoptosis may be involved in the pathogenesis of emphysema. Here, we describe an anmal model of emphysema characterized by airspace enlargement, alveolar wall destruction, the loss of elaston layers, and enhanced lung distensibility in mice receiving a sngle intratracheal ingection of active caspase-3 and chariot^<○R>, a newly developed protein transfection reagent. Epithehal apoptosis and enhanced elastolytc actualy in the bronchoalveolar lavage fluid and cells of these animals were noted.
Emphysema was also modeled in mice receiving an intratrocheal injection of nodularin, a proapoptotic sercne/threonine kirase inhibitor.
This murine model provides direct evidence conferming that alveolar wall apoptosis causes palmonary emphysema. Furtermore, this simple technique ofr the protein transfection of lung tissue can be used for a variety of future applications.
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