Genetic polymorphism in matrix metalloproteinase-9 and pulmonary emphysema
Genetic polymorphism in matrix metalloproteinase-9 and pulmonary emphysema
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DOI：
10.1006/bbrc.2001.5936
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发表时间：
2001-11-23
影响因子：
3.1
通讯作者：
Yamaguchi, K
中科院分区：
文献类型：
--
作者：
Minematsu, N;Nakamura, H;Yamaguchi, K
基因变异导致的蛋白酶-抗蛋白酶失衡可能是吸烟引起肺气肿的主要原因。由于基质金属蛋白酶（MMPs）最近被认为在肺气肿的发病机制中起重要作用，我们在日本对110名吸烟者和94名非吸烟者进行了MMP-9 （-1562C/T）功能多态性与肺气肿发展之间的关系进行了研究。胸部ct扫描有明显肺气肿的受试者（n = 45）的T等位基因频率高于无明显肺气肿的受试者（n = 65） （0.244 vs 0.123, P = 0.02）。Logistic回归分析显示，T等位基因是吸烟致肺气肿的危险因素（优势比= 2.69,P = 0.02）。C/T和T/T组（n = 35） DLCO/VA较C/C组（n = 75）低（P = 0.02），肺气肿变化明显（P = 0.03）。这些结果提示MMP-9的多态性是吸烟致肺气肿发生的遗传因素。(C) 2001学术出版社。
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. (C) 2001 Academic Press.