首页> 美国卫生研究院文献>Molecular Medicine Reports >miR-21-5p regulates type II alveolar epithelial cell apoptosis in hyperoxic acute lung injury
【2h】

miR-21-5p regulates type II alveolar epithelial cell apoptosis in hyperoxic acute lung injury

机译:miR-21-5p在高氧急性肺损伤中调节II型肺泡上皮细胞凋亡

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Hyperoxia-induced acute lung injury (HALI) as one of the most common complications in patents on mechanical ventilation, and there are no efficient methods to overcome this at present. It was hypothesized that microRNA 21-5p(miR-21-5p) can promote the survival of type II alveolar epithelial cells (AECII), alleviating HALI. The present study aimed to combine gene chip analysis with the overexpression miR-21-5p to develop a novel therapeutic option for HALI. It was found that AECII apoptosis was an important pathogenic event in the development of HALI, and the overexpression of miR-21-5p prevented HALI, associated with reducing AECII apoptosis. These results were obtained using adenoviral/lentiviral vectors, which overexpressed miR-21-5p, to transfect AECII cells in vitro and in vivo. It was found that the overexpression of miR-21-5p reduced the apoptotic rate of the AECII cells. In addition, miR-21-5p decreased the ratio of B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 and the expression of caspase-3. It was also revealed that the overexpression of miR-21-5p alleviated acute lung injury in adult rats exposed to a hyperoxic environment. These results suggest that miR-21-5p may become a novel therapeutic option for patients with HALI, by protecting AECII cells from apoptosis.
机译:高氧诱导的急性肺损伤(HALI)是机械通气专利中最常见的并发症之一,目前尚无有效的方法来克服。据推测,microRNA 21-5p(miR-21-5p)可以促进II型肺泡上皮细胞(AECII)的存活,减轻HALI。本研究旨在将基因芯片分析与过表达miR-21-5p结合起来,为HALI开发新的治疗选择。发现AECII凋亡是HALI发生中的重要致病事件,并且miR-21-5p的过表达阻止HALI,这与减少AECII凋亡有关。这些结果是使用过度表达miR-21-5p的腺病毒/慢病毒载体在体外和体内转染AECII细胞获得的。发现miR-21-5p的过表达降低了AECII细胞的凋亡率。此外,miR-21-5p降低了与B细胞淋巴瘤2(Bcl-2)相关的X蛋白/ Bcl-2的比例以及caspase-3的表达。还揭示了miR-21-5p的过表达减轻了暴露于高氧环境的成年大鼠的急性肺损伤。这些结果表明,通过保护AECII细胞免于凋亡,miR-21-5p可能成为HALI患者的新型治疗选择。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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