肺间质纤维化中去整合素金属蛋白酶17的表达及作用机制

Expression of disintegrin and metalloproteinase 17 and its mechanism in pulmonary fibrosis

目的观察去整合素金属蛋白酶17(ADAM17)在肺结节病、肺结核、非小细胞肺癌等肺间质纤维化疾病中差异表达情况,并探讨其作用机制。方法实时RT-PCR分别检测肺结节病、肺结核、肺癌和正常人的肺组织中ADAM17基因表达,采用Western blot方法检测相互作用因子-Ⅲ型胶原蛋白、整合素6的蛋白表达。结果肺组织中ADAM17 m RNA、Ⅲ型胶原蛋白、整合素6的蛋白在肺结节病组、肺结核组、非小细胞肺癌中的表达水平均明显高于正常对照组(P<0.05);肺癌组中以上指标的表达水平与正常对照组比较差异有统计学意义(P<0.01),与肺结节病组、肺结核组比较差异亦有统计学意义(P<0.05)。结论肺纤维化疾病的机制可能与ADAM17导致细胞外基质成员Ⅲ型胶原蛋白、整合素6的高表达有关。

[Objective] To investigate disintegrin and metalloproteinase （ADAM17） expression levels in sareoidosis, non-small cell lung cancer and tuberculosis, and to explore its mechanism. [Methods] Real-time PCR and Western blot were used respectively to measure the expressions of ADAM17 mRNA, Collagen In and Integrin 6 proteins in lung tissues of healthy volunteers （HV）, tuberculosis （TB） patients, lung cancer patients and sarcoidosis patients. [Results] The expressions of ADAM17 mRNA, Collagen Ⅲ and Integrin 6 proteins in the lung tissues of pulmonary sarcoidosis, tuberculosis and lung cancer patients were significantly higher than those in HV （P 〈 0.05）. The expression levels of the above indicators in the lung cancer group were significantly higher than those in the normal control group （P 〈 0.01）, and compared to those in the pulmonary sarcoidosis and tuberculosis groups there were also statistical differences （P 〈 0.05）. [ Conclusions ] Mechanisms of pulmonary fibrosis diseases may be correlated to the higher expressions of the extracellular matrix components collagen Ⅲ and integrin 6 induced by ADAMI7.