首页> 外文期刊>Journal of Huazhong University of Science and Technology >Activity of Matrix Metalloproteinase in Airway Epithelial Cells of COPD Patients
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Activity of Matrix Metalloproteinase in Airway Epithelial Cells of COPD Patients

机译:COPD患者气道上皮细胞中基质金属蛋白酶的活性

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摘要

To examine the mRNA expression of matrix metalloproteinase 9 (MMP-9) and the gelati-nase activity of its inhibitor, tissue inhibitor of matrix metalloproteinase 1 (TIMP-1) in the primary epithelial cells of patients with COPD, airway epithelial cells were taken from 15 COPD patients and cultured in vitro. The patients were divided into three groups, COPD group, normal smoking control group and non-smoking control group, with 5 subjects in each group, on basis of the smoking history and lung function. The semi-qualitative RT-PCR was employed to determine the mRNA levels of MMP-9 and TIMP-1 and SDS PAGE was used for the determination of the gelatinase activity of MMP-9 and TIMP-1. Our result showed that the mRNA of MMP-9 and TIMP-1 in epithelial cells of the non-smoking subjects was at a low level. The mRNA of MMP-9 and TIMP-1 in COPD patients and smokers was significantly higher than that in non-smokers (P < 0. 05). No significant difference was found in the levels of MMP-9 and TIMP-1 in epithelial cells between the COPD patients and smokers. The MMP-9/TIMP-1 ratios in COPD patients and smokers were significantly lower than that of non-smokers (P < 0. 05). The gelatinase activity in the epithelial cells of both COPD patients and normal smokers was increased (P < 0. 05) , but no difference existed in the gelatinase activity in the epithelial cells between COPD patients and normal smokers. It is concluded that the transcription of MMP-9 and TIMP-1 and the gelatinase activity of MMP-9 and MMP-2 in the epithelial cells in COPD patients were increased, which resulted in an imbalance of MMP-9/ TIMP-1, thereby causing pulmonary fibrosis. These factors play important roles in the pathogene-sis of COPD.
机译:为检测COPD患者原发上皮细胞,气道上皮细胞中基质金属蛋白酶9(MMP-9)的mRNA表达及其抑制剂的明胶酶活性,基质金属蛋白酶1的组织抑制剂(TIMP-1)。从15名COPD患者中进行体外培养。根据吸烟史和肺功能,将患者分为COPD组,正常吸烟对照组和非吸烟对照组三组,每组5名受试者。使用半定性RT-PCR确定MMP-9和TIMP-1的mRNA水平,并且使用SDS PAGE确定MMP-9和TIMP-1的明胶酶活性。我们的结果表明,非吸烟对象的上皮细胞中MMP-9和TIMP-1的mRNA水平较低。 COPD患者和吸烟者的MMP-9和TIMP-1的mRNA显着高于非吸烟者(P <0. 05)。在COPD患者和吸烟者之间,上皮细胞中MMP-9和TIMP-1的含量没有显着差异。 COPD患者和吸烟者的MMP-9 / TIMP-1比值显着低于非吸烟者(P <0. 05)。 COPD患者和正常吸烟者的上皮细胞中的明胶酶活性均升高(P <0. 05),但COPD患者和正常吸烟者的上皮细胞中的明胶酶活性无差异。结论:COPD患者上皮细胞中MMP-9和TIMP-1的转录以及MMP-9和MMP-2的明胶酶活性增加,导致MMP-9 / TIMP-1失衡,从而导致肺纤维化。这些因素在COPD的发病中起着重要作用。

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