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Abstract：
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 semiselective membrane for gas exchange. The miRNA miR-642a-5p has previously been reported to be up-regulated in patients with acute respiratory distress syndrome; 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 quantitative RT-PCR. 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 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and cell permeability was analyzed using the transendothelial electrical resistance assay. We report that miR-642a-5p levels are significantly up-regulated in LPS-stimulated PMVECs, and miR-642a-5p contributes to LPS-induced hyperpermeability and apoptosis of PMVECs. LPS treatment results in down-regulation 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/acute respiratory distress syndrome diagnosis or treatment.
摘要：
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