Abstract

Preeclampsia is a disease associated with developmental defects in the placenta. However, the pathogenesis of preeclampsia has not been precisely elucidated. Extensive studies have found that noncoding ribonucleic acid is involved in transcription and post-transcriptional translation. In the present study, we expounded on the pathogenic mechanism and diagnostic potential of noncoding ribonucleic acid in preeclampsia. We obtained the differentially expressed long noncoding ribonucleic acid urothelial carcinoma-associated 1 from the gene expression omnibus dataset. Urothelial carcinoma-associated 1 participated as a core gene in the construction of the competing endogenous ribonucleic acid network. The receiver operating characteristic curves were used to construct a diagnostic model for preeclampsia. Besides, the biological processes that urothelial carcinoma-associated 1 may influence in preeclampsia development were explored. Then, we detected urothelial carcinoma-associated 1, microRNA-18a, and hypoxia-inducible factor-1 alpha expressions by real-time quantitative polymer chain reaction and Western blotting. Based on the HTR-8/SVneo cell hypoxia model, we altered the expression of urothelial carcinoma-associated 1 or microRNA-18a by transfection. Cell counting kit-8, transwell, and wound healing assay were applied to treated cells to detect changes in their biological behaviors. Clinical samples confirmed that urothelial carcinoma-associated 1 and hypoxia-inducible factor-1 alpha messenger ribonucleic acid were more abundant in the placenta of patients with preeclampsia, while microRNA-18a was deficient. Urothelial carcinoma-associated 1 regulated the expression of hypoxia-inducible factor-1 alpha via microRNA-18a, promoting trophoblastic cell migration, invasion, and proliferation. Aspirin treatment significantly repaired the invasive function of drug-induced hypoxic trophoblasts, and the expression levels of these three genes were altered. Thus, we concluded that urothelial carcinoma-associated 1/microRNA-18a/hypoxia-inducible factor-1 alpha forms a molecular pathway that affects the biological behaviors of trophoblast cells and participates in the pathogenesis of preeclampsia.