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Long non-coding RNA SNHG5 suppresses the development of acute respiratory distress syndrome by targeting miR-205/COMMD1 axis

Molecular and Cellular Biochemistry volume 476, pages 1063–1074 (2021)Cite this article

Abstract

Previous studies have reported the important roles of long non-coding RNAs (lncRNAs) in acute respiratory distress syndrome (ARDS). Here, we focus on the role and regulatory mechanism of lncRNA SNHG5 in ARDS. LPS was used to induce mice to establish ARDS model in vivo and to induce A549 cells to establish ARDS model in vitro. qRT-PCR was performed to determine the expressions of SNHG5, miR-205, and inflammatory cytokines. MTT assay was applied to detect cell viability. Dual-luciferase reporter (DLR) assay was performed to test the interactions among SNHG5, miR-205 and COMMD1. Western blot was used to detect the protein expression of COMMD1. Lung injury was evaluated by evaluating the score of lung injury, lung wet/dry weight ratio, and myeloperoxidase (MPO) activity. SNHG5 was downregulated, while miR-205 was upregulated in the serum of ARDS patients and lung tissues of LPS-induced mice. Upregulation of SNHG5 or down-regulation of miR-205 inhibited inflammation and promoted the viability of LPS-induced A549 cells. SNHG5 alleviated the lung injury of ARDS mice. MiR-205 was a target of SNHG5 and inversely correlated with SNHG5. COMMD1 was targeted by miR-205, and was positively regulated by SNHG5. MiR-205 mimics or sh-COMMD1 reversed the promoting effect of SNHG5 on cell viability and the suppressing effect of SNHG5 on inflammation in cellular model of ARDS. Meantime, miR-205 mimics reversed the relieving effect of SNHG5 on lung injury in mouse model of ARDS. SNHG5 acted as a sponge for miR-205 to ameliorate LPS-induced ARDS by regulating COMMD1.

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All data in the manuscript is available through the responsible corresponding author.

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Funding

Heilongjiang Provincial Health and Family Planning Commission approved a scientific research Project, No. 2018-222. Project Name: Study on peripheral blood immune response of NRDS by HFOV combined with exogenous PS.

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Author notes

  1. Jiao Wang and Yang Zhang are co-first authors

Affiliations

  1. Department of Pediatric Medicine I, The First Affiliated Hospital of Jiamusi University, No. 348, Dexiang Street, Xiangyang District, Jiamusi City, 154002, Heilongjiang Province, China

    Jiao Wang & Yang Zhang

  2. Department of General Surgery I, The First Affiliated Hospital of Jiamusi University, No. 348, Dexiang Street, Xiangyang District, Jiamusi City, 154002, Heilongjiang Province, China

    Lihai Zhang

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  1. Jiao Wang
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  2. Yang Zhang
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  3. Lihai Zhang
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Contributions

JW and YZ: conception and design and analysis of data. JW, YZ and LZ: performed the experiment. JW and YZ: drafting the article. LZ: revising the article critically for important intellectual content. JW and YZ: performed the data. LZ: helped perform the analysis with constructive discussions. All the authors read and approved the manuscript.

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Correspondence to Lihai Zhang.

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This study was approved by the ethics committee of The First Affiliated Hospital of Jiamusi University. Written informed consent was obtained from all subjects.

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Wang, J., Zhang, Y. & Zhang, L. Long non-coding RNA SNHG5 suppresses the development of acute respiratory distress syndrome by targeting miR-205/COMMD1 axis. Mol Cell Biochem 476, 1063–1074 (2021). https://doi.org/10.1007/s11010-020-03972-8

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  • DOI: https://doi.org/10.1007/s11010-020-03972-8

Keywords

  • Acute respiratory distress syndrome
  • Acute lung injury
  • Long non-coding RNASNHG5
  • miR-205
  • COMMD1