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首页> 外文期刊>Journal of receptor and signal transduction research >Expression analysis of Akt and MAPK signaling pathways in lung tissue of patients with idiopathic pulmonary fibrosis (IPF)
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Expression analysis of Akt and MAPK signaling pathways in lung tissue of patients with idiopathic pulmonary fibrosis (IPF)

机译：特发性肺纤维化（IPF）患者肺组织中Akt和MAPK信号通路的表达分析

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Purpose of the study: Several studies in patients with lung cancer have shown that epidermal growth factor receptor regulates various tumorigenic processes through the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin and Ras/Raf/Mek/Erk (mitogen-activated protein kinase (MAPK)) signalling pathways. The aim of our study is to evaluate whether these pathways are implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and to seek indirect evidence of a common pathogenetic pathway with lung cancer. m-RNA expression of oncogenes participating in these two signaling pathways, as well as the combined m-RNA expression of the suppressor genes R-kip and p53 in lung tissue of patients with IPF were evaluated. Basic procedures: The study population was composed by two distinct groups. Patients with IPF (n25) and control subjects who underwent thoracic surgery for reasons other than interstitial lung disease (n10). Expression analysis of the aforementioned oncogenes and suppressor genes was performed using real-time reverse transcription polymerase chain reaction. Main findings: We found no difference in the overall m- RNA expression between controls and IPF in both investigated pathways. However, Braf has been overexpressed in IPF samples (P0.01) in contrast with K-ras that has been found downregulated (P<0.001) in comparison with controls. Principal conclusions: These findings cannot exclude the hypothesis of involvement of Akt and MAPK signalling pathways in pathogenesis of IPF. However, further investigation is needed in order to verify these data.
机译：研究目的：多项针对肺癌患者的研究表明，表皮生长因子受体通过雷帕霉素的磷酸肌醇3激酶/ Akt /哺乳动物靶标和Ras / Raf / Mek / Erk（促分裂原活化蛋白激酶）调节多种致瘤过程。 （MAPK））信号通路。我们研究的目的是评估这些途径是否与特发性肺纤维化（IPF）的发病机制有关，并寻找肺癌常见致病途径的间接证据。评价了参与这两个信号通路的癌基因的m-RNA表达，以及IPF患者肺组织中抑制基因R-kip和p53的联合m-RNA表达。基本程序：研究人群由两个不同的群体组成。患有IPF的患者（n25）和对照对象因间质性肺疾病（n10）以外的原因接受了胸外科手术。使用实时逆转录聚合酶链反应进行上述癌基因和抑制基因的表达分析。主要发现：我们发现在两种研究途径中，对照和IPF之间的总体m-RNA表达没有差异。然而，与K-ras相比，与对照相比，Braf在IPF样品中过表达（P0.01），而K-ras被下调（P <0.001）。主要结论：这些发现不能排除Akt和MAPK信号通路参与IPF发病的假说。但是，需要进一步调查以验证这些数据。

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