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Abstract

The incidence of pulmonary thromboembolism (PTE) has increased year on year, with high rates of misdiagnosis and recurrence, as well as significant heterogeneity in prognosis. This study investigated the clinical value of miR-183-5p in PTE, as well as its mechanism of regulating disease progression through PDCD4. This study enrolled 126 PTE patients and 103 non-PTE patients. Serum miR-183-5p was detected using qPCR, and its diagnostic and prognostic significance were analyzed using ROC and logistic analyses. A PTE cell model was established using 150 µg/mL ox-LDL. The effects of inhibiting only miR-183-5p, and co-inhibiting with PDCD4, on the HPMECs functions, inflammation/oxidative stress, and adhesion molecules were analyzed. Serum miR-183-5p in PTE patients increased gradually with risk stratification. The diagnostic efficacy of miR-183-5p for PTE was superior to that of D-dimer, and combining the two provides even better diagnostic results. miR-183-5p was an independent risk factor for prognosis in PTE patients. In a PTE cell model, inhibiting miR-183-5p restored HPMECs proliferation and suppressed apoptosis and autophagy. It also reduced the inflammatory factors release, alleviated oxidative stress damage and down-regulated the adhesion molecules expression. There was a direct target relationship between miR-183-5p and PDCD4. Co-suppression both miR-183-5p and PDCD4 reversed the hindering effect of inhibiting only miR-183-5p on PTE progression. miR-183-5p is a novel biomarker for the supplementary diagnosis and 30-day short-term prognosis assessment of PTE, and it participates in PTE progression by targeting PDCD4 to regulate vascular endothelial cell function.