Long non-coding RNA C1RL-AS1 aggravates influenza A virus pneumonia through miR-16-5p/LAMP3.

IF 1.9 4区医学 Q3 GENETICS & HEREDITY Virus Genes Pub Date : 2025-01-02 DOI:10.1007/s11262-024-02131-1

Xingjuan Liao, Qin Liang, Chao Xu, Xinbing Luo

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Abstract

Influenza A viruses continue to pose a serious threat to public health and economic stability. To investigate the role of C1RL-AS1 in influenza A virus (IAV) pneumonia. Using RT-qPCR analysis, we determined C1RL-AS1 expression levels in children with IAV-infected pneumonia and A549 cells. C1RL-AS1 expression levels in children were subjected to ROC analysis. C1RL-AS1 was knocked down to investigate its role in IAV-infected A549 cells, including effects on viral nucleoprotein (NP) production, cell survival, and apoptosis. Downstream miRNAs of C1RL-AS1 were predicted and validated. MiR-16-5p target genes were predicted and validated. C1RL-AS1 was up-regulated in IAV-infected children and A549 cells. C1RL-AS1 expression levels distinguished children with IAV pneumonia from healthy children. Knockdown of C1RL-AS1 attenuated viral NP production, promoted A549 cell survival, and inhibited apoptosis. MiR-16-5p was a downstream C1RL-AS1 miRNA. miR-16-5p counteracted the anti-IAV infection effect brought about by C1RL-AS1 knockdown. LAMP3 was a miR-16-5p target gene associated with pneumonia. LAMP3 restored the cellular effects brought about by C1RL-AS1/miR-16-5p co-knockdown. C1RL-AS1 is a possible diagnostic factor for IAV pneumonia in children. C1RL-AS1 may participate in IAV pneumonia by sponging miR-16-5p and then moderating LAMP3.

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长链非编码RNA C1RL-AS1通过miR-16-5p/LAMP3加重甲型流感病毒肺炎

甲型流感病毒继续对公共卫生和经济稳定构成严重威胁。目的探讨C1RL-AS1在甲型流感病毒（IAV）肺炎中的作用。采用RT-qPCR分析，我们检测了iav感染的肺炎患儿和A549细胞中C1RL-AS1的表达水平。对患儿的C1RL-AS1表达水平进行ROC分析。研究人员敲除了C1RL-AS1，以研究其在iav感染的A549细胞中的作用，包括对病毒核蛋白（NP）产生、细胞存活和凋亡的影响。预测并验证了C1RL-AS1的下游mirna。预测并验证MiR-16-5p靶基因。在iav感染儿童和A549细胞中，C1RL-AS1表达上调。C1RL-AS1表达水平可区分IAV肺炎患儿与健康儿童。敲低C1RL-AS1可降低病毒NP的产生，促进A549细胞存活，抑制细胞凋亡。MiR-16-5p是下游的C1RL-AS1 miRNA。miR-16-5p抵消了C1RL-AS1敲低带来的抗iav感染作用。LAMP3是与肺炎相关的miR-16-5p靶基因。LAMP3恢复了C1RL-AS1/miR-16-5p共敲低所带来的细胞效应。C1RL-AS1可能是儿童IAV肺炎的诊断因子。C1RL-AS1可能通过海绵化miR-16-5p，然后调节LAMP3参与IAV肺炎。

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来源期刊

Virus Genes 医学-病毒学

CiteScore

3.30

自引率

0.00%

发文量

审稿时长

3 months

期刊介绍： Viruses are convenient models for the elucidation of life processes. The study of viruses is again on the cutting edge of biological sciences: systems biology, genomics, proteomics, metagenomics, using the newest most powerful tools. Huge amounts of new details on virus interactions with the cell, other pathogens and the hosts – animal (including human), insect, fungal, plant, bacterial, and archaeal - and their role in infection and disease are forthcoming in perplexing details requiring analysis and comments. Virus Genes is dedicated to the publication of studies on the structure and function of viruses and their genes, the molecular and systems interactions with the host and all applications derived thereof, providing a forum for the analysis of data and discussion of its implications, and the development of new hypotheses.