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Background   Idiopathic pulmonary fibrosis (IPF), the most common interstitial lung disease, arises from transforming growth factor beta 1- (TGF β 1-) induced aberrant fibroproliferation in response to epithelial injury. The TGF β 1-) induced aberrant fibroproliferation in response to epithelial injury. The TGF    Methods   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.Results   Lung tissue microarray data mining and immunohistochemistry revealed significantly downregulation of  HYAL1  in IPF lung tissue. However,  HYAL1  in IPF lung tissue. However,  HYAL1  in IPF lung tissue. However,  HYAL1  in IPF lung tissue. However,  β 1-) induced aberrant fibroproliferation in response to epithelial injury. The TGF β 1-) induced aberrant fibroproliferation in response to epithelial injury. The TGF    Conclusions   We showed that  HYAL1  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. HYAL1  in IPF lung tissue. However,

HYAL1 Is Downregulated in Idiopathic Pulmonary Fibrosis and Inhibits HFL-1 Fibroblast Proliferation When Upregulated