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首页> 外文期刊>Frontiers in Cell and Developmental Biology >Progression of Pulmonary Emphysema and Continued Increase in Ectodomain Shedding of Cell Adhesion Molecule 1 After Cessation of Cigarette Smoke Exposure in Mice
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Progression of Pulmonary Emphysema and Continued Increase in Ectodomain Shedding of Cell Adhesion Molecule 1 After Cessation of Cigarette Smoke Exposure in Mice

机译：小鼠卷烟烟雾暴露后细胞粘附分子1肺肺部肺肺部进展和外枝瘤脱落的继续增加

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Pulmonary emphysema usually arises in cigarette smokers, and often progresses after smoking cessation and even in ex-smokers. Lung-epithelial cell adhesion molecule 1 (CADM1), an immunoglobulin superfamily member, is extracellularly shed to produce a proapoptotic C-terminal fragment (CTF) within the cell and contribute to the development of emphysema. Here, we made an ex-smoker model using C57BL/6 mice; mice (6-week-old; 5 mice per group) were exposed to passive smoke of eight cigarettes twice a day 5 days a week until 18 weeks of age, and were then left untreated until 30 weeks of age. We calculated the mean linear intercept (Lm) and the alveolar septal thickness in the lung histologic sections to estimate the alveolar space dilatation. At 18 weeks of age, Lm was marginally enlarged (P = 0.023) with a marked increase in the septal thickness (P < 0.001) in comparison with age-matched control mice (5 mice per group), while at 30 weeks, the increase in Lm was much more prominent (P = 0.006) and the septal thickness was normalized, suggesting that emphysema progressed with septal remodeling during smoking cessation. Western blot analyses of the lungs were performed for CADM1, a possible CADM1 sheddase ADAM10, an epithelial marker pan-cytokeratin, and a myofibroblastic marker α-smooth muscle actin to estimate the expression levels of CTF and ADAM10 per epithelial cell and the levels of pan-cytokeratin and αSMA per tissue. CADM1 shedding was increased in the treated mice than in control mice at both ages, in association with an increase in the CTF level at 30 weeks (P = 0.021). In total of the treated and control mice of 30 weeks of age, Lm was positively correlated with the CTF and ADAM10 levels, and pan-cytokeratin was negatively correlated with CTF, suggesting an involvement of CADM1 shedding in emphysema progression. Positive correlations were also found between CTF and ADAM10, and between ADAM10 and αSMA, suggesting that increased septal myofibroblasts might be involved in increased CADM1 shedding. Taken together, persisting increase in ectodomain shedding of CADM1 appeared to contribute to the progression of emphysema in ex-smokers, and might be accounted for by alveolar septal remodeling.
机译：肺气肿通常在吸烟者中出现，并且在吸烟后经常进展，甚至在出吸烟者中。肺上皮细胞粘附分子1（CADM1），一种免疫球蛋白超家族成员，是细胞外落的，以在细胞内产生促凋亡C末端片段（CTF），并有助于肺气肿的发展。在这里，我们使用C57BL / 6只小鼠进行了出吸烟模型;小鼠（6周龄;每组5只小鼠）暴露于每周5天的每天两次暴露于八支香烟的被动烟雾，直到18周龄，然后在30周龄之前留下了未经处理的。我们计算了肺组织学区中的平均线性截距（LM）和肺泡隔膜厚度，以估计肺泡空间扩张。在18周龄时，LM略微扩大（p = 0.023），与年龄匹配对照小鼠（每组5只小鼠）相比，平间厚度（P <0.001）的显着增加（P <0.001），而在30周内增加在LM中更加突出（p = 0.006）并且正常化的间隔厚度，表明在吸烟期间肺气肿进展了隔膜。对CADM1进行肺部的蛋白质印迹分析，可能的CADM1 Sheddase ADAM10，上皮标记泛细胞角蛋白和肌纤维囊肿标记物α-平滑肌肌动蛋白，以估计每个上皮细胞的CTF和ADAM10的表达水平和锅的水平-Cytokeratin和αsma每组。在治疗的小鼠中增加了CADM1脱落，而不是两年龄段的对照小鼠，与30周的CTF水平的增加（P = 0.021）。总共30周龄的治疗和对照小鼠，LM与CTF和ADAM10水平呈正相关，泛细胞角蛋白与CTF与CTF呈负相关，表明CADM1脱落在肺气肿进展中的参与。在CTF和ADAM10之间以及ADAM10和αsma之间也发现了阳性相关性，表明增加的隔膜肌纤维素可能涉及增加的CADM1脱落。连同，持续增加突突脱落的CADM1似乎有助于出吸烟者肺气肿的进展，并且可能会被肺泡隔膜重塑所占。

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