ArticleMolecular medicine reports2018
RNA‑sequencing analysis of aberrantly expressed long non‑coding RNAs and mRNAs in a mouse model of ventilator‑induced lung injury.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- The emerging regulatory roles of non-coding RNA in Ventilator-induced Lung Injury.Non-coding RNA research · 2026Review
- Microarray analysis of hub genes, non-coding RNAs and pathways in lung after whole body irradiation in a mouse model.International journal of radiation biology · 2023Article
- The impact of bacterial exposure in early life on lung surfactant gene expression, function and respiratory rate in germ-free mice.Frontiers in microbiomes · 2023Article
- Long non-coding RNA NEAT1 participates in ventilator-induced lung injury by regulating miR-20b expression.Molecular medicine reports · 2022Article
- Ventilator-induced lung-injury in mouse models: Is there a trap?Laboratory animal research · 2021Review
- Mining the key genes for ventilator-induced lung injury using co-expression network analysis.Bioscience reports · 2021Article
- Article
- Prenatal Cadmium Exposure Alters Proliferation in Mouse CD4Frontiers in immunology · 2021Article
- Transcriptome-Wide Gene Expression in a Murine Model of Ventilator-Induced Lung Injury.Disease markers · 2021Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (lncRNAs) are closely associated with the regulation of various biological processes and are involved in the pathogenesis of numerous diseases. However, to the best of our knowledge, the role of lncRNAs in ventilator‑induced lung injury (VILI) has yet to be evaluated. In the present study, high‑throughput sequencing was applied to investigate differentially expressed lncRNAs and mRNAs (fold change >2; false discovery rate <0.05). Bioinformatics analysis was employed to predict the functions of differentially expressed lncRNAs. A total of 104 lncRNAs (74 upregulated and 30 downregulated) and 809 mRNAs (521 upregulated and 288 downregulated) were differentially expressed in lung tissues from the VILI group. Gene ontology analysis demonstrated that the differentially expressed lncRNAs and mRNAs were mainly associated with biological functions, including apoptosis, angiogenesis, neutrophil chemotaxis and skeletal muscle cell differentiation. The top four enriched pathways were the tumor necrosis factor (TNF) signaling pathway, P53 signaling pathway, neuroactive ligand‑receptor interaction and the forkhead box O signaling pathway. Several lncRNAs were predicted to serve a vital role in VILI. Subsequently, three lncRNAs [mitogen‑activated protein kinase kinase 3, opposite strand (Map2k3os), dynamin 3, opposite strand and abhydrolase domain containing 11, opposite strand] and three mRNAs (growth arrest and DNA damage‑inducible α, claudin 4 and thromboxane A2 receptor) were measured by reverse transcription‑quantitative polymerase chain reaction, in order to confirm the veracity of RNA‑sequencing analysis. In addition, Map2k3os small interfering RNA transfection inhibited the expression of stretch‑induced cytokines [TNF‑α, interleukin (IL)‑1β and IL‑6] in MLE12 cells. In conclusion, the results of the present study provided a profile of differentially expressed lncRNAs in VILI. Several important lncRNAs may be involved in the pathological process of VILI, which may be useful to guide further investigation into the pathogenesis for this disease.
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