miR-642a-5p partially mediates the effects of lipopolysaccharide on human pulmonary microvascular endothelial cells via eEF2.
miR-642a-5p partially mediates the effects of lipopolysaccharide on human pulmonary microvascular endothelial cells via eEF2.
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miR-642a-5p通过EEF2部分介导脂多糖对人肺微血管内皮细胞的影响。
DOI：
10.1002/2211-5463.12969
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发表时间：
2020-11
期刊：
影响因子：
2.6
通讯作者：
You Q
中科院分区：
文献类型：
--
作者：
Fei L;Sun G;You Q
miR-642a-5p 通过靶向真核延伸因子 2 促进脂多糖诱导的通透性过高和细胞凋亡。因此，miR-642a-5p 和真核延伸因子 2 可能是急性肺损伤/急性呼吸窘迫综合征诊断或治疗的潜在靶点。 吸入或全身给予脂多糖（LPS）可诱发急性肺部炎症和肺损伤。肺血管系统由肺微血管内皮细胞（PMVEC）组成，形成用于气体交换的半选择性膜。此前有报道称，miRNA miR-642a-5p 在急性呼吸窘迫综合征患者中表达上调；因此，在这里，我们检查了该 miRNA 是否参与 LPS 对 PMVEC 的影响。通过定量 RT-PCR 检测 miR-642a-5p 和编码真核延伸因子 2 (eEF2) 的 mRNA 水平。通过蛋白质印迹法检测 Moesin 和 eEF2 蛋白水平。双荧光素酶报告基因测定用于检查 miR-642a-5p 和 eEF2 之间的关系。使用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物测定评估细胞活力，并使用跨内皮电阻测定分析细胞通透性。我们报告说，在 LPS 刺激的 PMVEC 中，miR-642a-5p 水平显着上调，并且 miR-642a-5p 有助于 LPS 诱导的 PMVEC 通透性过高和凋亡。 LPS 治疗导致 PMVEC 中 eEF2 下调。 eEF2（miR-642a-5p 的直接靶标）的过度表达抑制 LPS 对 PMVEC 的作用。 miR-642a-5p 通过靶向 eEF2 促进 LPS 诱导的通透性过高和细胞凋亡。因此，miR-642a-5p和eEF2可能作为急性肺损伤/急性呼吸窘迫综合征诊断或治疗的潜在靶点。
miR‐642a‐5p promotes lipopolysaccharide‐induced hyperpermeability and apoptosis by targeting eukaryotic elongation factor 2. Thus, miR‐642a‐5p and eukaryotic elongation factor 2 may be potential targets for acute lung injury/acute respiratory distress syndrome diagnosis or treatment. 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.
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影响因子：
64.8
作者：
Lu, J;Getz, G;Golub, TR
通讯作者：
Golub, TR
影响因子：
3.7
作者：
Ma C;Zhang W;Wu Q;Liu Y;Wang C;Lao G;Yang L;Liu P
通讯作者：
Liu P
影响因子：
6.1
作者：
Ling, Yun;Li, Zheng-Zhao;Zhang, Jian-Feng;Zheng, Xiao-Wen;Lei, Zhuo-Qing;Chen, Ru-Yan;Feng, Ji-Hua
通讯作者：
Feng, Ji-Hua
影响因子：
5.1
作者：
Jiang, Wenjiao;Luo, Fen;Ding, Xuansheng
通讯作者：
Ding, Xuansheng
影响因子：
5.1
作者：
Luh Shi-Ping;Chiang Chi-Huei
通讯作者：
Chiang Chi-Huei