...
首页> 外文期刊>Journal of Cellular Physiology >Poly r(C) binding protein 1‐mediated regulation of microRNA expression underlies post‐sevoflurane amelioration of acute lung injury in rats
【24h】

Poly r(C) binding protein 1‐mediated regulation of microRNA expression underlies post‐sevoflurane amelioration of acute lung injury in rats

机译:保利r (C)结合蛋白1介导的监管microRNA表达基础岗位应承担的七氟醚改良的大鼠急性肺损伤

获取原文
获取原文并翻译 | 示例
           

摘要

Acute lung injury (ALI) presents a pervasive health burden due to the high morbidity and mortality associated with it. Volatile anesthetics like sevoflurane has been previously shown to have organ‐protective effect, both in the context of normal physiological function in liver, and during LPS‐induced ALI. Sevoflurane was shown to exert lung protective effect during LPS‐induced ALI by modulating expression level of microRNAs (miRNAs), specifically miR‐155. The objective of the current study was to define the underlying mechanism by which sevoflurane alters miRNA expression levels. Lung injury caused by LPS and its amelioration post sevoflurane administration was first confirmed. Expression levels of different miRNA and messenger RNAs (mRNAs) encoding inflammatory cytokines were measured in a rat model of lipopolysaccharide (LPS)‐induced ALI, which were subsequently treated with either sevoflurane or vehicle control. Host of miRNAs and messenger RNAs encoding pro‐inflammatory cytokines are overexpressed during LPS‐induced ALI, which are reversed following sevoflurane administration. Mass spectrometry analysis revealed that the RNA‐binding protein, poly r(C) binding protein 1 (PCBP1) expression is induced in ALI and is repressed following sevoflurane treatment. RNA immunoprecipitation experiments revealed that PCBP1 expression dictates the altered miRNA expression and sevoflurane altered miRNA expression by suppressing PCBP1 expression. Our study thus elucidates a unique mechanism of lung protective effect of sevoflurane mediated by suppression of expression of a RNA‐binding protein that potentiates expression of pro‐inflammatory miRNAs.
机译:急性肺损伤(ALI)提出了一种无处不在由于高发病率和卫生负担与之相关的死亡率。麻醉药七氟醚已经像以前发现机关应承担的保护作用,无论是正常的生理功能肝脏,在LPS诱导阿里。期间被证明产生肺保护作用LPS诱导ALI的调制表达水平小分子核糖核酸(microrna),特别是米尔155。当前研究的目的是为了定义七氟醚改变底层机制microrna的表达水平。有限合伙人及其改进后七氟醚政府第一次被证实。不同的microrna和信使rna水平(mrna)编码炎性细胞因子用脂多糖的大鼠模型(有限合伙人)高诱导ALI在随后七氟烷或处理控制。地理编码pro炎性细胞因子的过表达在LPS诱导ALI应承担的逆转后七氟醚。质谱分析表明地理RNA结合蛋白,保利r (C)结合蛋白1(PCBP1)表达式是在阿里和诱导压抑后七氟醚治疗。免疫沉淀反应的实验显示,PCBP1表达决定了microrna的改变表达和七氟醚microrna的改变表达抑制PCBP1表达式。研究从而阐明了肺的一个独特的机制七氟醚介导的保护作用抑制RNA表达的绑定强化表达的蛋白质pro‐inflammatory鉴定。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号