Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.
Cell Biochem Biophys. 2024 Jun;82(2):1135-1143. doi: 10.1007/s12013-024-01264-2. Epub 2024 Apr 18.
Acute respiratory distress syndrome (ARDS) is regarded as a type of respiratory failure. Emerging evidence has demonstrated the significant roles of microRNAs in various disorders. Nevertheless, the role of miR-202-3p in ARDS is unclear. Forty male C57BL/6 mice treated with phosphate buffer saline/lipopolysaccharide (PBS/LPS) and administrated with NC/miR-202-3p agomir were divided into four groups. A reverse transcription-quantitative polymerase chain reaction was used to evaluate the level of miR-202-3p, its target genes, and proinflammatory factors. Hematoxylin‑eosin was utilized for histological observation of the lung tissues. The Wet/Dry ratio, myeloperoxidase activity, and total protein concentration in bronchoalveolar lavage fluid were assessed to determine pulmonary edema. Western blotting was used for quantifying protein levels of proinflammatory factors, nuclear factor kappa B (NF-κB), and NLR family pyrin domain containing 3 (NLRP3) signaling-associated proteins. Calmodulin 1 (Calm1) protein expression in murine lung tissues was evaluated by immunohistochemistry. The binding relation between miR-202-3p and Calm1 was assessed by luciferase reporter assay. The results showed that miR-202-3p was lowly expressed in the lung tissues of ARDS mice. Overexpressed miR-202-3p relieved LPS-induced edema, reduced proinflammatory factors, and inactivated NF-κB/NLRP3 signaling in murine lung tissues. Calm1 was targeted by miR-202-3p and displayed a high level of LPS-induced ARDS. In conclusion, miR-202-3p targets Calm1 and suppresses inflammation in LPS-induced ARDS, thereby inhibiting the pathogenesis of ARDS in a mouse model.
急性呼吸窘迫综合征（ARDS）被认为是一种呼吸衰竭。新出现的证据表明，microRNAs 在各种疾病中起着重要作用。然而，miR-202-3p 在 ARDS 中的作用尚不清楚。40 只雄性 C57BL/6 小鼠用磷酸盐缓冲盐水/脂多糖（PBS/LPS）处理，并给予 NC/miR-202-3p agomir 处理，分为四组。使用逆转录定量聚合酶链反应评估 miR-202-3p、其靶基因和促炎因子的水平。苏木精-伊红用于肺组织的组织学观察。评估湿/干比、髓过氧化物酶活性和支气管肺泡灌洗液中的总蛋白浓度以确定肺水肿。Western blotting 用于定量炎症因子、核因子 kappa B（NF-κB）和 NOD 样受体家族 pyrin 结构域包含 3（NLRP3）信号相关蛋白的蛋白水平。通过免疫组织化学评估鼠肺组织中钙调蛋白 1（Calm1）蛋白的表达。通过荧光素酶报告测定评估 miR-202-3p 与 Calm1 的结合关系。结果表明，miR-202-3p 在 ARDS 小鼠的肺组织中低表达。过表达 miR-202-3p 可减轻 LPS 诱导的水肿，减少促炎因子，并使鼠肺组织中的 NF-κB/NLRP3 信号失活。Calm1 是 miR-202-3p 的靶标，并且在 LPS 诱导的 ARDS 中显示出高水平。总之，miR-202-3p 靶向 Calm1 并抑制 LPS 诱导的 ARDS 中的炎症，从而抑制小鼠模型中 ARDS 的发病机制。
