LINC02605 通过 miR-539-5p/CXCL1 轴参与小儿肺炎支原体肺炎并发腹泻的研究。

IF 4.4 3区 医学 Q1 MEDICINE, GENERAL & INTERNAL
Yang Zhang, Zeming Wu
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引用次数: 0

摘要

背景为了研究LINC02605在小儿肺炎支原体肺炎(MPP)进展过程中的参与作用,我们招募了132名肺炎支原体肺炎患儿(90名单纯肺炎支原体肺炎患儿和42名肺炎支原体肺炎+腹泻患儿),并收集他们的血浆以检测LINC026505的表达。采用 CCK-8 试剂盒和商业凋亡试剂盒检测细胞生长和凋亡。在通过双荧光素酶报告实验验证后,进行了硅预测分析,以预测 LINC02605 的下游 miRNA。结果LIN02605在MPP中高表达,尤其是在并发腹泻的MPP中。LINC02605 在 A549 细胞中的下调与细胞凋亡率和体外生长抑制率的显著抑制相关。在含有野生型 LINC02605 和 CXCL1 的报告系统中,引入 miR-539-5p 可抑制荧光素酶活性。经 LAMPs 刺激后,发现 LINC02605 和 CXCL1 过表达,miR-539-5p 受抑制,miR-539-5p 和 CXCL1 的敲除对 LINC02605 抑制的细胞凋亡有挽救作用。结论LINC02605在MPP中上调,miR-539-5p是LINC02605的靶标。LINC02605可能参与了胃肠道和呼吸道之间的串联。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

LINC02605 involved in paediatric Mycoplasma pneumoniae pneumonia complicated with diarrhoea via miR-539-5p/CXCL1 axis

LINC02605 involved in paediatric Mycoplasma pneumoniae pneumonia complicated with diarrhoea via miR-539-5p/CXCL1 axis

Background

To investigate the involvement of LINC02605 in the progression of paediatric Mycoplasma pneumoniae pneumonia (MPP).

Methods

One hundred and thirty-two children with MPP (90 simple MPP and 42 MPP + diarrhoea) were enrolled, and their plasma was collected for detection of LINC026505 expression. CCK-8 kit and commercial apoptosis kit were introduced to determine cell growth and apoptosis. In silico prediction analyses were conducted to predict the downstream miRNA for LINC02605, following verification by dual luciferase reporter assay. The lipid-associated membrane proteins (LAMPs) were used to treat A549 and Coca-2 cells.

Results

LIN02605 was highly expressed in the MPP, especially in MPP complicated with diarrhoea. LINC02605 downregulation in A549 cells correlated with significant suppression of cell apoptosis rate and growth inhibition rate in vitro. Introduction of miR-539-5p inhibited luciferase activity in a reporter system containing the wild-type LINC02605 and CXCL1. After stimulation with LAMPs, overexpression of LINC02605 and CXCL1 and inhibition of miR-539-5p were found. miR-539-5p and CXCL1 knockdown resulted in a rescue effect on the LINC02605-inhibited cell apoptosis. LAMPs induced IL-1β in intestinal epithelial cells and IL-1β induced LINC02605 expression in A549 cells.

Conclusions

LINC02605 was upregulated in MPP and miR-539-5p was a target for LINC02605. LINC02605 may be involved in the crosstalk between the gastrointestinal tract and the respiratory tract.

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来源期刊
CiteScore
9.50
自引率
3.60%
发文量
192
审稿时长
1 months
期刊介绍: EJCI considers any original contribution from the most sophisticated basic molecular sciences to applied clinical and translational research and evidence-based medicine across a broad range of subspecialties. The EJCI publishes reports of high-quality research that pertain to the genetic, molecular, cellular, or physiological basis of human biology and disease, as well as research that addresses prevalence, diagnosis, course, treatment, and prevention of disease. We are primarily interested in studies directly pertinent to humans, but submission of robust in vitro and animal work is also encouraged. Interdisciplinary work and research using innovative methods and combinations of laboratory, clinical, and epidemiological methodologies and techniques is of great interest to the journal. Several categories of manuscripts (for detailed description see below) are considered: editorials, original articles (also including randomized clinical trials, systematic reviews and meta-analyses), reviews (narrative reviews), opinion articles (including debates, perspectives and commentaries); and letters to the Editor.
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