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Background    Sepsis, a type of systemic disease, can impact nearly all organs, tissues and cells. Among them, endothelial cells are amongst the first to be affected and respond to the insult. In this study, we investigated the protective effects of microRNA-30a-5p (miR-30a-5p) on human pulmonary microvascular endothelial cells (HPMECs) treated with lipolysaccharide (LPS).Methods    An  in vitro  model of sepsis was established in HPMECs with the use of LPS. Transfecting with different tools (mimetic and inhibitor) to modify miR-30a-5p expression. Cell viability, proliferation and apoptosis were detected by the CCK-8 assay, the EdU kit and fluorescence staining, respectively. The autophagy-related protein and mRNA expression, the number of autophagosomes were separately examined through Western blot analysis, qPT-PCR and confocal microscopy. TargetScan and the luciferase reporter assays were used to probe target genes interacting with miR-30a-5p.Results    LPS caused a reduction in the viability and proliferation of HPMECs, as well as an elevation in the number of apoptotic cells. Subsequently, we observed that miR-30a-5p might play a role in preventing LPS-induced inhibition of cell damage and decreasing HPMEC apoptosis, suggesting the potential function of miR-30a-5p in this injury process. Finally, we confirmed that miR-30a-5p exerts its protective effect by regulating cell autophagy, possibly by targeting Beclin-1.Conclusion    Our study provided evidence that autophagy is a crucial aspect in the protective role of miR-30a-5p against LPS-induced HPMEC injury, identifying a promising target for sepsis-related endothelial cell injury.

MiR-30a-5p alleviates LPS-induced HPMEC injury through regulation of autophagy via Beclin-1