MicroRNAs associated with smoking-induced pulmonary emphysema in senescence marker protein-30 knockout mice

吸烟是慢性阻塞性肺疾病（COPD）最重要的病因，但其发病机制尚不完全清楚。我们以前曾报道，衰老标记蛋白-30基因敲除（SMP 30-KO）小鼠可用于研究香烟烟雾诱导的肺气肿。此外，我们已经证明miR-146 a在COPD的异常炎症反应中起致病作用。在暴露于稀释的香烟烟雾或新鲜空气2周期间，在第1天和第8天鼻内给予维生素C控制的SMP 30-KO miR-146 a抑制剂。miR-146 a抑制剂和烟雾暴露小鼠的BALF中总细胞和淋巴细胞数量均增加。PGE 2的产生和考克斯-2的表达也增加了显着更高的暴露两种miR-146 a抑制剂和香烟烟雾。总之，miR-146 a似乎在异常炎症反应在吸烟暴露的COPD小鼠模型中发挥致病作用。

Cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD), but the mechanisms of pathogenesis are incompletely defined. We have previously reported that senescence marker protein-30 knockout (SMP30-KO) mice can be useful for investigating cigarette smoke-induced pulmonary emphysema. Moreover, we have already shown that miR-146a plays a pathogenetic role in the abnormal inflammatory response in COPD.Vitamin C-controlled SMP30-KO were given miR-146a inhibitor on day 1 and 8 intranasally during exposure to either diluted cigarette smoke or fresh air for 2 weeks. Total cell and lymphocyte numbers were increased in the BALF of both miR-146a inhibitor and smoke exposed mice. PGE2 production and COX-2 expression were also increased significantly higher by exposure both miR-146a inhibitor and cigarette smoke.In conclusion, miR-146a appears to play a pathogenetic role in the abnormal inflammatory response in a cigarette smoke-exposed murine model of COPD.