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Updated: Jun 4, 2025
Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition
Published on: June 10, 2016
ANGPTL4 mediated mesothelial-mesenchymal transition in pulmonary fibrosis: a potential therapeutic target
Yuechong Xia1, Fang Zhou2, Hongyan Hui2
1Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Background:
Glycolysis plays a major role in progression of idiopathic pulmonary fibrosis (IPF). Here, we aim to explore the predictive signature based on glycolysis-related genes for predicting the prognosis and identified a potential therapeutic target for IPF.
Methods:
Gene expression data of bronchoalveolar lavage (BAL) cells and clinical information were downloaded from the Gene Expression Omnibus database. Bioinformatic analysis was then performed to identify differentially expressed genes (DEGs). Lasso multivariate cox analysis and multivariate Cox regression were used to establish a gene signature. The prediction model was evaluated using the time-dependent receiver operating characteristic (ROC) curve and validated using an external independent dataset. The expression of these key genes in cellular level analyzed from Single Cell Expression Atlas. Cell Counting Kit-8 assay, immunofluorescence, wound healing and plasmid transfection were performed.
Results:
A total of 4 gene (ANGPTL4, ME2, TPBG and IER3), which were associated with the prognosis of IPF patients, were selected to establish our signature. The prediction model was an independent prognostic indicator for IPF patients. ANGPTL4 was significantly upregulated in pleural mesothelial cells (PMCs). In vitro assay showed that ANGPTL4 promoted PMCs proliferation and migration. Knockdown of ANGPTL4 can inhibit mesothelial-mesenchymal transition by suppressed glycolysis-associated gene, such as PGM1, GPI, PGK1, LDHA, ALDOA, ENO1 and TPI1.
Conclusions:
Our research established a glycolysis-associated gene signature that holds potential to assist clinicians in the personalized management of IPF. Furthermore, we identified that ANGPTL4 mediates mesothelial-mesenchymal transition, suggesting its viability as a therapeutic target for IPF treatment.
