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首页> 美国卫生研究院文献>American Journal of Respiratory Cell and Molecular Biology >Temporal and Spatial Expression of Transforming Growth Factor-β after Airway Remodeling to Tobacco Smoke in Rats
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Temporal and Spatial Expression of Transforming Growth Factor-β after Airway Remodeling to Tobacco Smoke in Rats

机译：大鼠烟气重塑后转化生长因子β的时空表达

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摘要

Airway remodeling is strongly correlated with the progression of chronic obstructive pulmonary disease (COPD). In this study, our goal was to characterize progressive structural changes in site-specific airways, along with the temporal and spatial expression of transforming growth factor (TGF)-β in the lungs of male spontaneously hypertensive rats exposed to tobacco smoke (TS). Our studies demonstrated that TS-induced changes of the airways is dependent on airway generation and exposure duration for proximal, midlevel, and distal airways. Stratified squamous epithelial cell metaplasia was evident in the most proximal airways after 4 and 12 weeks but with minimal levels of TGF-β–positive epithelial cells after only 4 weeks of exposure. In contrast, epithelial cells in midlevel and distal airways were strongly TGF-β positive at both 4 and 12 weeks of TS exposure. Airway smooth muscle volume increased significantly at 4 and 12 weeks in midlevel airways. Immunohistochemistry of TGF-β was also found to be significantly increased at 4 and 12 weeks in lymphoid tissues and alveolar macrophages. ELISA of whole-lung homogenate demonstrated that TGF-β2 was increased after 4 and 12 weeks of TS exposure, whereas TGF-β1 was decreased at 12 weeks of TS exposure. Airway levels of messenger RNA for TGF-β2, as well as platelet-derived growth factor-A, granulocyte-macrophage colony–stimulating factor, and vascular endothelial growth factor-α, growth factors regulated by TGF-β, were significantly decreased in animals after 12 weeks of TS exposure. Our data indicate that TS increases TGF-β in epithelial and inflammatory cells in connection with airway remodeling, although the specific role of each TGF-β isoform remains to be defined in TS-induced airway injury and disease.
机译：气道重塑与慢性阻塞性肺疾病（COPD）的进展密切相关。在这项研究中，我们的目标是表征特定部位气道中进行性的结构变化，以及在暴露于烟草烟雾（TS）的雄性自发性高血压大鼠肺中转化生长因子（TGF）-β的时空表达。我们的研究表明，TS引起的气道变化取决于气道的产生以及近端，中水平和远端气道的暴露时间。暴露4周和12周后，在最近端的气道中可见分层的鳞状上皮细胞化生，但仅暴露4周后，TGF-β阳性的上皮细胞水平最低。相反，在TS暴露的4周和12周时，中，上呼吸道的上皮细胞均为强TGF-β阳性。中层气道在第4和12周时，气道平滑肌体积显着增加。在淋巴组织和肺泡巨噬细胞中，TGF-β的免疫组织化学在第4周和第12周时也显着增加。全肺匀浆的ELISA结果表明，TS暴露4周和12周后TGF-β2升高，而TS暴露12周时TGF-β1降低。 TGF-β2的信使RNA的气道水平以及血小板衍生的生长因子-A，粒细胞-巨噬细胞集落刺激因子和血管内皮生长因子-α（受TGF-β调节的生长因子）均显着降低TS暴露12周后。我们的数据表明，与气道重塑相关的TS增加了上皮细胞和炎性细胞中的TGF-β，尽管每种TGF-β同工型的具体作用在TS诱导的气道损伤和疾病中仍有待确定。

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