Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, The Ohio State University Wexner Medical Center, 473 West 12th Avenue, Columbus, OH, 43210, USA.
Department of Biomedical Engineering, The Ohio State University, 140 West 19th Avenue, Columbus, OH, 43210, USA.
Nat Commun. 2021 Jan 12;12(1):289. doi: 10.1038/s41467-020-20449-w.
Mechanical ventilation generates injurious forces that exacerbate lung injury. These forces disrupt lung barrier integrity, trigger proinflammatory mediator release, and differentially regulate genes and non-coding oligonucleotides including microRNAs. In this study, we identify miR-146a as a mechanosensitive microRNA in alveolar macrophages that has therapeutic potential to mitigate lung injury during mechanical ventilation. We use humanized in-vitro systems, mouse models, and biospecimens from patients to elucidate the expression dynamics of miR-146a needed to decrease lung injury during mechanical ventilation. We find that the endogenous increase in miR-146a following injurious ventilation is not sufficient to prevent lung injury. However, when miR-146a is highly overexpressed using a nanoparticle delivery platform it is sufficient to prevent injury. These data indicate that the endogenous increase in microRNA-146a during mechanical ventilation is a compensatory response that partially limits injury and that nanoparticle delivery of miR-146a is an effective strategy for mitigating lung injury during mechanical ventilation.
机械通气会产生损伤性力,从而加重肺损伤。这些力会破坏肺屏障的完整性,触发促炎介质的释放,并对基因和非编码寡核苷酸(包括 microRNA)进行差异调控。在这项研究中,我们确定 miR-146a 是肺泡巨噬细胞中的一种机械敏感性 microRNA,具有减轻机械通气期间肺损伤的治疗潜力。我们使用人源化的体外系统、小鼠模型和来自患者的生物样本,阐明了在机械通气期间降低肺损伤所需的 miR-146a 的表达动力学。我们发现,损伤性通气后内源性 miR-146a 的增加不足以预防肺损伤。然而,当使用纳米颗粒递送平台高度过表达 miR-146a 时,足以预防损伤。这些数据表明,机械通气期间 microRNA-146a 的内源性增加是一种代偿性反应,部分限制了损伤的发生,而纳米颗粒递送 miR-146a 是减轻机械通气期间肺损伤的有效策略。