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首页> 外文期刊>Balkan journal of medical genetics: BJMG >ASSOCIATION OF THE MMP7-181A G PROMOTER POLYMORPHISM WITH EARLY ONSET OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE
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ASSOCIATION OF THE MMP7-181A G PROMOTER POLYMORPHISM WITH EARLY ONSET OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

机译：MMP7-181A＆GT的关联。 G启动子多态性与慢性阻塞性肺病的早期发作

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Chronic obstructive pulmonary disease (COPD) is characterized by decreased air flow and is associated with abnormal chronic inflammation in the airways and extensive tissue remodeling. Matrix metalloproteinase-7 (MMP7) is produced primarily by the epithelium of many organs, including the lungs. A functional MMP7 -181AG (rs11568818) promoter polymorphism influences the binding of nuclear regulatory proteins modulating the transcription of the gene. In this study, we genotyped 191 patients with COPD for MMP7 -181AG single nucleotide polymorphism (SNP) and 215 control subjects using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and explored the role of that polymorphism as a risk factor for COPD. There were no differences in the genotype and allele distribution of the MMP7 -181AG SNP between the COPD patients and control groups (p = 0.341 and p = 0.214). However, the carries of the G allele (AG and GG genotypes), appeared to develop COPD significantly earlier than those with the AA genotype (61.01 +/- 10.11 vs. 64.87 +/- 9.00 years, p = 0.032). When the genotype distribution was studied only in the groups of patients (n = 76) and controls (n = 106) younger than 60 years, we found significantly higher frequency of the carriers of the G allele in COPD patients than in the controls, determining about a 3-fold higher risk for COPD [odds ratio (OR) -3.33, 1.36-8.14, p = 0.008 for GG, and OR = 2.91, 1.38-6.13, p = 0.005 for AG+GG]. Based on our results, the MMP7 -181AG promoter variant may influence early development of COPD. This effect could be attributed to the increased production of the enzyme resulting in enhanced airway wall protein degradation and injury.
机译：慢性阻塞性肺疾病（COPD）的特征在于空气流量下降，并且与气道中的慢性炎症异常和广泛的组织重塑相关。基质金属蛋白酶-7（MMP7）主要由许多器官的上皮产生，包括肺部。功能性MMP7 -181A＆GT; G（RS11568818）启动子多态性影响核调节蛋白调节基因转录的结合。在这项研究中，我们使用聚合酶链反应限制片段长度多态性（PCR-RFLP）方法的单核苷酸多态性（SNP）和215对照受试者进行191例COPD患者。 COPD的危险因素。在COPD患者和对照组之间MMP7 -181A＆GT的基因型和等位基因分布没有差异（P = 0.341和P = 0.214）。然而，具有G等位基因（AG和GG基因型）的携带显着提前显着显着发育COPD（61.01 +/- 10.11与64.87 +/- 9.00岁，P = 0.032）。当基因型分布仅在患者组（n = 76）和60岁的对照组（n = 106）中时，我们发现COPD患者G等位基因的载体频率明显高于控制，确定对于COPD的风险高出3倍[差距（或）-3.33,1.36-8.14，P = 0.008，GG，或= 2.91,1.38-6.13，P = 0.005对于Ag + Gg]。基于我们的结果，MMP7 -181A＆GT; G启动子变体可能会影响COPD的早期发展。这种效果可归因于增加酶的产生，导致气道壁蛋白质的增强和损伤。

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