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Heterogeneous response of nasal and lung fibroblasts to transforming growth factor-β1

机译：鼻和肺成纤维细胞对转化生长因子-β1的异质反应

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Background: Nasal polyposis is characterized by marked oedema, sparse extracellular matrix (ECM) and proliferating blood vessels. Pulmonary fibrosis is characterized by inflammatory cells accumulation, considerable ECM deposition and vascular abnormalities. Although lung fibrosis is not only and necessarily an inflammatory disorder, we hypothesized that the difference between nasal polyposis and pulmonary fibrosis may, in part, be due to the heterogeneity between nasal and lung fibroblasts. Fibroblasts participate in the inflammatory response by releasing ECM proteins and cytokines. TGF-? is thought to participate in chronic inflammation and fibrosis. Myofibroblasts are the activated form of fibroblasts. A phenotypic hallmark of myofibroblasts is the expression of smooth muscle ?-actin (SMA). Objective: We examined whether there is any heterogeneity between nasal and lung fibroblasts upon stimulation with TGF-?with regard to the synthesis of SMA, pro-collagen type I and vascular endothelial growth factor (VEGF) as well as translocation of Smad proteins. Methods: Fibroblasts lines were established from human biopsy tissue. The expression of SMA, pro-collagen type I, VEGF mRNA was evaluated by reverse transciptase RT-PCR. The amount of pro-collagen type I and VEGF was measured by ELISA. By immunocytochemistry, we analysed the expression of SMA and Smad2, 3, 4 in cultured fibroblasts. Results: TGF-?induced SMA and pro-collagen type I synthesis in lung, but not in nasal fibroblasts. By contrast, TGF-?induced VEGF synthesis in both lung and nasal fibroblasts. After stimulation with TGF-? Smad2, 3, 4 were translocated from the cytoplasm to the nucleus in lung fibroblasts, whereas only Smad3 was translocated in nasal fibroblasts. Conclusion: These results establish the heterogeneous responsiveness of fibroblast populations in the airways to TGF-?and that such a heterogeneity may contribute, at least in part, to the different pathological outcomes of inflammation in the upper and lower airways.
机译：背景：鼻息肉病的特征是明显的水肿，稀疏的细胞外基质（ECM）和血管增生。肺纤维化的特征是炎性细胞积聚，大量ECM沉积和血管异常。尽管肺纤维化不仅是而且不一定是炎性疾病，但我们假设鼻息肉病和肺纤维化之间的差异可能部分是由于鼻和肺成纤维细胞之间的异质性引起的。成纤维细胞通过释放ECM蛋白和细胞因子参与炎症反应。 TGF-？被认为参与慢性炎症和纤维化。肌成纤维细胞是成纤维细胞的活化形式。成肌纤维细胞的表型特征是平滑肌β-肌动蛋白（SMA）的表达。目的：我们检查了TGF-β刺激后鼻和肺成纤维细胞在SMA的合成，I型胶原原和血管内皮生长因子（VEGF）的合成以及Smad蛋白的转运方面是否存在异质性。方法：从人体活检组织中建立成纤维细胞系。通过逆转录酶RT-PCR评估SMA，I型胶原原，VEGF mRNA的表达。通过ELISA测量I型胶原原和VEGF的量。通过免疫细胞化学，我们分析了培养的成纤维细胞中SMA和Smad2、3、4的表达。结果：TGF-β诱导的SMA和I型胶原原在肺中合成，但在鼻成纤维细胞中则不合成。相反，TGF-β诱导肺和鼻成纤维细胞中的VEGF合成。用TGF-β刺激后？ Smad2、3、4在肺成纤维细胞中从细胞质转移到细胞核，而仅Smad3在鼻成纤维细胞中转移。结论：这些结果建立了气道中成纤维细胞群对TGF-β的异质性反应，这种异质性可能至少部分地导致上，下气道炎症的不同病理结果。

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