ArticleJournal of cellular and molecular medicine2021
MiR-144-induced KLF2 inhibition and NF-kappaB/CXCR1 activation promote neutrophil extracellular trap-induced transfusion-related acute lung injury.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- IL-36 activates neutrophil extracellular traps and exacerbates LPS-induced ARDS in mice.Scientific reports · 2026Article
- TRIM30a coordinates neutrophil-macrophage crosstalk to resolve inflammation and drive osseointegration via suppressing NETosis/cGAS-STING axis.Materials today. Bio · 2026Article
- miR-320d Is Associated with Reduced Nasopharyngeal Carcinoma Progression, Potentially through the NF-κB/IL-8 Axis-Mediated Inhibition of Neutrophil Extracellular Trap Formation.Oncology research · 2026Article
- miRNAs-neutrophil axis: novel insights into acute lung injury and chronic inflammatory lung diseases.Frontiers in immunology · 2026Review
- miR-144/451: A Regulatory Role in Inflammation.Current molecular medicine · 2025Review
- KLF2 controls the apoptosis of neutrophils and is associated with disease activity of systemic lupus erythematosus.Arthritis research & therapy · 2024Article
- Mechanism of KLF2 in young mice with pneumonia induced by Streptococcus pneumoniae.Journal of cardiothoracic surgery · 2024Article
- A Narrative Review: The Role of NETs in Acute Respiratory Distress Syndrome/Acute Lung Injury.International journal of molecular sciences · 2024Review
- Hypobaric Hypoxia Aggravates Renal Injury by Inducing the Formation of Neutrophil Extracellular Traps through the NF-κB Signaling Pathway.Current medical science · 2023Article
- Postoperative hypoxemia for patients undergoing Stanford type A aortic dissection.World journal of clinical cases · 2023Review
- Neutrophil extracellular traps and their implications in airway inflammatory diseases.Frontiers in medicine · 2023Review
- Crosstalk between neutrophil extracellular traps and immune regulation: insights into pathobiology and therapeutic implications of transfusion-related acute lung injury.Frontiers in immunology · 2023Review
- Inflammatory microRNAs in cardiovascular pathology: another brick in the wall.Frontiers in immunology · 2023Review
- Update on transfusion-related acute lung injury: an overview of its pathogenesis and management.Frontiers in immunology · 2023Review
- MiR-144-induced KLF2 inhibition and NF-kappaB/CXCR1 activation promote neutrophil extracellular trap-induced transfusion-related acute lung injury.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transfusion-related acute lung injury (TRALI) is a clinical syndrome which is associated with the formation of neutrophil extracellular trap (NET). Recent studies have demonstrated the roles of microRNAs (miRNAs) in the pathophysiological process of TRALI. Here, the study focused on the role of miR-144 and the molecular mechanisms in NET-induced TRALI. Up-regulated miR-144 and under-expressed KLF2 were determined in patients with TRALI. In the mouse model of a two-event TRALI induced by intraperitoneal injections with lipopolysaccharide and anti-H-2Kd mAb, we determined expression patterns of miR-144, Krüppel-like factor 2 (KLF2), chemokine (C-X-C motif) receptor 1 (CXCR1) and nuclear factor kappa-B (NF-kappaB) p65. The results confirmed that miR-144 was highly expressed, while KLF2 was poorly expressed in mice with TRALI. Dual-luciferase reporter gene assay identified that miR-144 could target KLF2. Using gain- and loss-of-function approaches, we analysed the effects of miR-144 and its interaction with KLF2 on TRALI. Enforced expression of miR-144 was found to aggravate NET-induced TRALI by down-regulating KLF2 and activating the NF-kappaB/CXCR1 signalling pathway in TRALI mice. Collectively, miR-144-targeted inhibition of KLF2 and activation of NF-kappaB/CXCR1 are possible mechanisms responsible for NET-caused TRALI. These findings aid in the development of therapeutic modalities for the treatment of TRALI.
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