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长链非编码 RNA MEG3 的上调表达可作为重症肺炎患儿的预后生物标志物及其调控机制。

Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism.

机构信息

Department of Neonatology, Yidu Central Hospital of Weifang, Weifang, Shandong, 262500, China.

Department of Neonatology, Weifang People's Hospital, Weifang, Shandong, 261041, China.

出版信息

Bioengineered. 2021 Dec;12(1):7120-7131. doi: 10.1080/21655979.2021.1979351.

Abstract

Severe pneumonia is a high-mortality disorder in children. The expression and underlying effects of lncRNA maternally expressed 3 (MEG3) were detected. The relationships between MEG3 and other parameters were reported by Pearson correlation. The prognostic importance of MEG3 was assessed by Kaplan-Meier (K-M) curve and COX analysis and its diagnostic potential was uncovered by the receiver operating characteristic (ROC) curve. Luciferase activity assay was performed to demonstrate the target gene of MEG3. Elevated expression of MEG3 and reduced microRNA-29 c (miR-29 c) were evaluated in severe pneumonia children, and a negative relationship between MEG3 and miR-29 c was propounded. MEG3 might function as an independent prognostic indicator. The diagnostic efficiency of MEG3 was also indicated for severe pneumonia children. In MRC-5 cell models and MH-S cell models, lipopolysaccharide (LPS) contributed to the increased expression of MEG3. Interference of MEG3 restricted the upregulation of MEG3 triggered by LPS. Silenced MEG3 protected MRC-5 and MH-S cells against damages managed by LPS on cell apoptosis, viability, and inflammation. MiR-29 c was a ceRNA of MEG3 and the absence of MEG3 abrogated the decreased expression of miR-29 c caused by LPS. Overall, the increased expression of MEG3 and the reduced levels of miR-29 c were identified in severe pneumonia. Prognostic and diagnostic significances of MEG3 provided a novel perspective for severe pneumonia. Disruption of MEG3 alleviated cell injury and inflammation as characterized by high LPS by binding miR-29 c.

摘要

严重肺炎是儿童高死亡率疾病。检测长链非编码 RNA 母源表达基因 3(MEG3)的表达和潜在作用。通过皮尔逊相关分析报告 MEG3 与其他参数的关系。通过 Kaplan-Meier(K-M)曲线和 COX 分析评估 MEG3 的预后重要性,并通过接收者操作特征(ROC)曲线揭示其诊断潜力。进行荧光素酶活性测定以证明 MEG3 的靶基因。评估严重肺炎患儿中 MEG3 的高表达和 microRNA-29c(miR-29c)的降低,并提出 MEG3 与 miR-29c 之间的负相关关系。MEG3 可能作为独立的预后指标。还表明 MEG3 对严重肺炎患儿的诊断效率。在 MRC-5 细胞模型和 MH-S 细胞模型中,脂多糖(LPS)导致 MEG3 的表达增加。MEG3 的干扰限制了 LPS 引发的 MEG3 的上调。沉默 MEG3 可防止 LPS 对 MRC-5 和 MH-S 细胞的细胞凋亡、活力和炎症造成损害。miR-29c 是 MEG3 的 ceRNA,MEG3 的缺失消除了 LPS 引起的 miR-29c 的表达降低。总体而言,在严重肺炎中发现 MEG3 的表达增加和 miR-29c 的水平降低。MEG3 的预后和诊断意义为严重肺炎提供了新的视角。通过与 miR-29c 结合,破坏 MEG3 可缓解由高 LPS 引起的细胞损伤和炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5525/8806474/9e87b3056290/KBIE_A_1979351_F0001_B.jpg

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