Clinical Laboratory, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Medical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Biomed Res Int. 2020 Mar 11;2020:3659451. doi: 10.1155/2020/3659451. eCollection 2020.
Idiopathic pulmonary fibrosis (IPF), the most common interstitial lung disease, arises from transforming growth factor beta 1- (TGF1-) induced aberrant fibroproliferation in response to epithelial injury. The TGF1-) induced aberrant fibroproliferation in response to epithelial injury. The TGF.
We first performed microarray data mining of previously published gene expression datasets to identify key gene signatures in IPF lung tissues. HYAL1 expression levels in IPF and normal lung tissues were then characterized using immunohistochemistry followed by real-time quantitative reverse transcription-PCR (qRT-PCR) and western blot analysis on isolated fibroblasts from fresh lung tissues of IPF and healthy donors. A human fetal lung fibroblast HFL-1 cell line, which was used in place of primary lung fibroblasts, was used to assess the proliferative or apoptotic effects associated with lentiviral-induced HYAL1 overexpression using CCK-8 cell proliferation assay and Annexin V-APC staining. The identification of potentially associated molecular pathways was performed using microarray analysis followed by qRT-PCR and western blot analysis.
Lung tissue microarray data mining and immunohistochemistry revealed significantly downregulation of in IPF lung tissue. However, in IPF lung tissue. However, in IPF lung tissue. However, in IPF lung tissue. However, 1-) induced aberrant fibroproliferation in response to epithelial injury. The TGF1-) induced aberrant fibroproliferation in response to epithelial injury. The TGF.
We showed that overexpression could prevent HFL-1 fibroproliferation. Furthermore, our findings suggest that transcriptional regulators and BMP receptor signaling may be involved in HYAL1 modulation in IPF therapy. in IPF lung tissue. However.
特发性肺纤维化（IPF）是最常见的间质性肺病，源于转化生长因子-β1（TGF-β1）诱导的上皮损伤后异常纤维增生。
我们首先对先前发表的基因表达数据集进行了微阵列数据挖掘，以鉴定 IPF 肺组织中的关键基因特征。然后通过免疫组织化学、实时定量逆转录-PCR（qRT-PCR）和来自 IPF 和健康供体新鲜肺组织的分离成纤维细胞的 Western blot 分析来描述 IPF 和正常肺组织中的 HYAL1 表达水平。我们使用人胎肺成纤维细胞 HFL-1 细胞系（代替原代肺成纤维细胞）来评估与慢病毒诱导的 HYAL1 过表达相关的增殖或凋亡效应，使用 CCK-8 细胞增殖测定和 Annexin V-APC 染色。通过微阵列分析、qRT-PCR 和 Western blot 分析来鉴定潜在相关的分子途径。
肺组织微阵列数据挖掘和免疫组织化学显示，在 IPF 肺组织中显著下调。然而，在 IPF 肺组织中。然而，在 IPF 肺组织中。然而，在 IPF 肺组织中。然而，1-) 诱导上皮损伤后的异常纤维增生。TGF-β1-) 诱导上皮损伤后的异常纤维增生。TGF-β1-) 诱导上皮损伤后的异常纤维增生。TGF-β1-) 诱导上皮损伤后的异常纤维增生。TGF-β1-) 诱导上皮损伤后的异常纤维增生。
我们表明，HYAL1 过表达可以阻止 HFL-1 成纤维细胞增殖。此外，我们的研究结果表明，转录调节剂和 BMP 受体信号可能参与 IPF 治疗中的 HYAL1 调节。
