ArticleMolecular therapy. Nucleic acids2020
Kcnq1ot1/miR-381-3p/ETS2 Axis Regulates Inflammation in Mouse Models of Acute Respiratory Distress Syndrome.
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
- Long non coding RNAs reveal important pathways in childhood asthma: a future perspective.Journal of molecular histology · 2023Review
- Long noncoding RNA signatures in intrauterine infection/inflammation-induced lung injury: an integrative bioinformatics study.BMC pulmonary medicine · 2023Article
- microRNA-145-5p attenuates acute lung injury via targeting ETS2.The Kaohsiung journal of medical sciences · 2022Article
- Long noncoding RNA Kcnq1ot1 prompts lipopolysaccharide-induced acute lung injury by microRNA-7a-5p/Rtn3 axis.European journal of medical research · 2022Article
- The downregulation of miR-129-5p relieves the inflammatory response in acute respiratory distress syndrome by regulating PPARγ-mediated autophagy.Annals of translational medicine · 2022Article
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- Potential of long non-coding RNA KCNQ1OT1 as a biomarker reflecting systemic inflammation, multiple organ dysfunction, and mortality risk in sepsis patients.Journal of clinical laboratory analysis · 2021Article
- Long non-coding RNAExperimental and therapeutic medicine · 2021Article
- Silencing of long non-coding RNA KCNQ1OT1 alleviates LPS-induced lung injury by regulating the miR-370-3p/FOXM1 axis in childhood pneumonia.BMC pulmonary medicine · 2021Article
- STAT3-activated lncRNA XIST accelerates the inflammatory response and apoptosis of LPS-induced acute lung injury.Journal of cellular and molecular medicine · 2021Article
- SNHG15 knockdown inhibits diabetic nephropathy progression in pediatric patients by regulating the miR-141/ICAM-1 axis in vitro.Bioscience reports · 2021Article
- Silencing Long Non-coding RNA Kcnq1ot1 Limits Acute Kidney Injury by Promoting miR-204-5p and Blocking the Activation of NLRP3 Inflammasome.Frontiers in physiology · 2021Article
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- Upregulation of matrix metalloproteinase 9 (MMP9)/tissue inhibitor of metalloproteinase 1 (TIMP1) and MMP2/TIMP2 ratios may be involved in lipopolysaccharide-induced acute lung injury.The Journal of international medical research · 2020Article
- CircHIPK3/miR-381-3p axis modulates proliferation, migration, and glycolysis of lung cancer cells by regulating the AKT/mTOR signaling pathway.Open life sciences · 2020Article
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Corrections and comments
- Retraction · 2022-05-10Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Paper Mill · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory mediators play a key role in the pathogenesis of acute respiratory distress syndrome (ARDS). In this study, we aimed to explore the involvement of the Kcnq1 opposite strand/antisense transcript 1 (Kcnq1ot1)/miR-381-3p/E26 transformation-specific proto-oncogene 2 (ETS2) axis in inflammation of lipopolysaccharide (LPS)-induced ARDS. Microarray analysis revealed ETS2 as an upregulated gene in ARDS. Then, a LPS-induced ARDS mouse model was constructed, with a series of gain- or loss-of-function experiments conducted to evaluate the lung function and neutrophil extracellular trap (NET) formation in lung tissue and determine the neutrophil number, myeloperoxidase (MPO) activity, and inflammatory factor levels in bronchoalveolar lavage fluid (BALF). As the results revealed, downregulated expression of ETS2 resulted in improved lung function, decreased NETs, MPO activity, and levels of interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α), as well as increased IL-10 level. Then, the assays of dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP), and RNA pull-down were performed to validate that Kcnq1ot1 promoted ETS2 expression by competitively binding to miR-381-3p. Meanwhile, it was also found that Kcnq1ot1 silencing reversed the promotive effect of EST2 on ARDS. Our results provide evidence that Kcnq1ot1 silencing may reduce the inflammatory response in LPS-induced ARDS via inhibition of miR-381-30-dependent ETS2, thereby presenting new molecular understanding for the development of ARDS.
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