MiR-642a-5p partially mediates the effects of lipopolysaccharide on human pulmonary microvascular endothelial cells via eEF2.
2020
Inhalation or systemic administration of lipopolysaccharide (LPS) can induce acute pulmonary inflammation and lung injury. The pulmonary vasculature is composed of pulmonary microvascular endothelial cells (PMVECs), which form a semi-selective membrane for gas exchange. The microRNA miR-642a-5p has previously been reported to be upregulated in patients with acute respiratory distress syndrome (ARDS), and thus here we examined whether this miRNA is involved in the effects of LPS on PMVECs. The levels of miR-642a-5p and mRNA encoding eukaryotic elongation factor 2 (eEF2) were detected by RT-qPCR. Moesin and eEF2 protein levels were tested by western blot assay. Dual-luciferase reporter assay was used to examine the relationship between miR-642a-5p and eEF2. Cell viability was assessed using the MTT assay, and cell permeability was analyzed using the transendothelial electrical resistance assay. We report that miR-642a-5p levels are significantly upregulated in LPS-stimulated PMVECs, and miR-642a-5p contributes to LPS-induced hyperpermeability and apoptosis of PMVECs. LPS treatment results in downregulation of eEF2 in PMVECs. Overexpression of eEF2, a direct target of miR-642a-5p, inhibited the effect of LPS on PMVECs. MiR-642a-5p promoted LPS-induced hyperpermeability and apoptosis by targeting eEF2. Thus, miR-642a-5p and eEF2 may serve as potential targets for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) diagnosis or treatment.
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