Genetic Polymorphism in Matrix Metalloproteinase-9 and Pulmonary Emphysema

• Published in: Biochemical and biophysical research communications Vol. 289; no. 1; pp. 116 - 119
• Main Authors: Minematsu, Naoto, Nakamura, Hidetoshi, Tateno, Hiroki, Nakajima, Takahiro, Yamaguchi, Kazuhiro
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 23.11.2001
• Subjects: Adult; Aged; Alleles; Case-Control Studies; Female; Gene Frequency; genetic polymorphism; Humans; Japan; Male; Matrix Metalloproteinase 9 - genetics; matrix metalloproteinase-9; Middle Aged; Polymorphism, Genetic; Pulmonary Disease, Chronic Obstructive - enzymology; Pulmonary Disease, Chronic Obstructive - etiology; Pulmonary Disease, Chronic Obstructive - genetics; pulmonary emphysema; Pulmonary Emphysema - enzymology; Pulmonary Emphysema - etiology; Pulmonary Emphysema - genetics; Risk Factors; smoking; Smoking - adverse effects; Japan; matrix metalloproteinase-9; genetic polymorphism; pulmonary emphysema; smoking
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1006/bbrc.2001.5936

Protease-antiprotease imbalance due to genetic variation may be responsible for the development of pulmonary emphysema induced by smoking. Since matrix metalloproteinases (MMPs) have recently been suggested to play important roles in the pathogenesis of pulmonary emphysema, the association between the functional polymorphism of MMP-9 (−1562C/T) and the development of pulmonary emphysema was examined in 110 smokers and 94 nonsmokers in Japan. The T allele frequency was higher in subjects with distinct emphysema on chest CT-scans (n = 45) than in those without it (n = 65) (0.244 vs 0.123, P = 0.02). Logistic regression analysis demonstrated that the T allele is a risk factor for smoking-induced emphysema (odds ratio = 2.69, P = 0.02). DLCO/VA was lower (P = 0.02) and emphysematous changes were more conspicuous (P = 0.03) in subjects with C/T or T/T (n = 35) than in those with C/C (n = 75). These results suggest that the polymorphism of MMP-9 acts as a genetic factor for the development of smoking-induced pulmonary emphysema.