Abstract

BackgroundAt present, the role of lncRNAs in the pathogenesis of hypoxia-induced pulmonary hypertension (HPH) is not fully understood. This study aimed to explore differences in the hypoxia-induced expression of lncRNAs and their potential role in multiple pulmonary artery cells.MethodsLncRNA expression in pulmonary artery smooth muscle cells (PASMCs), pulmonary microvascular endothelial cells (PMECs), and pericytes (PCs) was analyzed by high-throughput sequencing and compared between normoxic and hypoxic cells. Bioinformatics analysis was conducted to predict their functions.ResultsPASMCs, PMECs, and PCs displayed 275 (140 upregulated), 251 (162 upregulated), and 290 (176 upregulated) different lncRNAs, respectively. Among these, lncRNA TUG1 levels increased in PASMCs and PCs but decreased in PMECs. Bioinformatics analysis indicated that lncRNA TUG1 might target miR-145-5p, thereby affecting SOX4 and BMF expression, and could also regulate miR-129-5p levels to affect CYP1B1 and VCP expression. It could also regulate miR-138-5p levels to affect KCNK3 and RHOC expression.ConclusionsHypoxia exposure of vascular cells resulted in differential expression of lncRNAs, especially lncRNA TUG1, which showed significant abnormal expression in all three types of vascular cells under hypoxia. Our results suggested that abnormal expression of lncRNA TUG1 might be involved in the regulation of pulmonary vascular cell function under hypoxia.

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