2003 Fiscal Year Final Research Report Summary
Role of EMMPRIN/basigm in the lung
| Project/Area Number |
14570532
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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 | HOKKAIDO UNIVERSITY |
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Principal Investigator |
BETSUYAKU Tomoko Hokkaido Univ., Medical Hospital, Assist.Prof., 医学部・歯学部附属病院, 講師 (60333605)
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| Project Period (FY) |
2002 – 2003
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| Keywords | smoking / fibrosis / gene / epithelium / bleomycin / pulmonary emphysema / macrophage / bronchoalveolar lavage |
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| Research Abstract |
Extracellular matrix metalloproteinase inducer (EMMPRIN), also called basigin, is present in the lung during development, but its expression in normal adult lung is minimal. Increases of EMMPRIN have been found in various forms of experimental lung injury. To determine whether EMMPRIN might be involved in alveolar injury/repair associated with smoking, we developed an enzyme-linked immunosoibent assay for EMMPRIN and applied it to bronchoalveolar lavage (BAL) fluids from never-smokers (n=7), former smokers (n=16) and current smokers (n=58). The smoker groups included subjects with emphysema as determined by high-resolution chest computed tomography. EMMPRIN levels were significantly elevated in current and former smokers, 315±20 and 175±15pg/ml SEM, respectively, compared to 31±7pg/ml in never-smokers, but the EMMPRIN levels of smokers with emphysema were not different from smokers without emphysema. Immunohistochemistry of smokers' lung tissue showed EMMPRIN in bronchiolar epithelium and alveolar macrophages, but EMMPRIN mRNA m alveolar macrophages was not different between current and never-smokers. Matrix metallopioteinase-1 was also detectable in the BAL fluid from some smokers, but not in never-smokers. These findings indicate that smoking is associated with increased intrapulmonary EMMPRIN. Whether EMMPRIN is involved in smoking-induced lung pathology remains to be determined.
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