ArticleCell cycle (Georgetown, Tex.)2019
Inhibition of miR-221 alleviates LPS-induced acute lung injury via inactivation of SOCS1/NF-κB signaling pathway.
Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- [Aerobic exercise regulates macrophage polarization and improves insulin resistance in mice: the mediating role of miR-221-3p].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Review
- Tiny Guides, Big Impact: Focus on the Opportunities and Challenges of miR-Based Treatments for ARDS.International journal of molecular sciences · 2024Review
- Dynamic changes in radiological parameters, immune cells, selected miRNAs, and cytokine levels in peripheral blood of patients with severe COVID‑19.Biomedical reports · 2023Article
- Treatment of Acute Respiratory Distress Syndrome Caused by COVID-19 with Human Umbilical Cord Mesenchymal Stem Cells.International journal of molecular sciences · 2023Article
- Active Fraction of Polyrhachis Vicina Roger (AFPR) Ameliorate Depression Induced Inflammation Response by FTO/miR-221-3p/SOCS1 Axis.Journal of inflammation research · 2023Article
- Sex-biased expression of selected chromosome x-linked microRNAs with potent regulatory effect on the inflammatory response in children with cystic fibrosis: A preliminary pilot investigation.Frontiers in immunology · 2023Article
- Epithelial‑derived exosomes promote M2 macrophage polarization via Notch2/SOCS1 during mechanical ventilation.International journal of molecular medicine · 2022Article
- microRNA-145-5p attenuates acute lung injury via targeting ETS2.The Kaohsiung journal of medical sciences · 2022Article
- Genes, environment, and developmental timing: New insights from translational approaches to understand early origins of respiratory diseases.Pediatric pulmonology · 2021Article
- MiR-221-3p and miR-92a-3p enhances smoking-induced inflammation in COPD.Journal of clinical laboratory analysis · 2021Article
- Diagnostic Values of miR-221-3p in Serum and Cerebrospinal Fluid for Post-Stroke Depression and Analysis of Risk Factors.Iranian journal of public health · 2021Article
- Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway.Bioscience reports · 2021Article
- A Blood Exosomal miRNA Signature in Acute Respiratory Distress Syndrome.Frontiers in molecular biosciences · 2021Article
- MiR-221/SIRT1/Nrf2 signal axis regulates high glucose induced apoptosis in human retinal microvascular endothelial cells.BMC ophthalmology · 2020Article
- Long Noncoding RNA SOCS2-AS Promotes Leukemogenesis in FLT3-ITD+ Acute Myeloid Leukemia Through miRNA-221.OncoTargets and therapy · 2020Article
- Innate Immune Memory in Macrophages.Newborn (Clarksville, Md.)Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of inflammation response has been well documented in the development of acute lung injury (ALI). However, little is known about the functions of miRNAs in the regulation of inflammation in ALI. The aim of this study was to explore the effects of miRNAs in the regulation of inflammation in ALI and to elucidate the biomolecular mechanisms responsible for these effects. The expression profiles of miRNAs in lung tissues from lipopolysaccharide (LPS)-induced ALI mice model were analyzed using a microarray. It was observed that microRNA-221-3p (miR-221) was significantly increased in lung tissues in ALI mice. The inhibition of miR-221 attenuated lung injury including decreased lung W/D weight ratio and lung permeability and survival rates of ALI mice, as well as apoptosis, whereas its agomir-mediated upregulation exacerbated the lung injury. Concomitantly, miR-221 inhibition significantly reduced LPS-induced pulmonary inflammation, while LPS-induced pulmonary inflammation was aggravated by miR-221 upregulation. Of note, suppressor of cytokine signaling-1 (SOCS1), an effective suppressor of the NF-κB signaling pathway, was found to be a direct target of miR-221 in RAW264.7 cells. Overexpression of SOCS1 by pcDNA-SOCS1 plasmids markedly reversed the miR-221 inhibition-mediated inhibitory effects on inflammation and apoptosis in LPS-treated RAW264.7 cells. Finally, it was found that miR-221 inhibition suppressed LPS induced the activation of the NF-κB signaling pathway, as demonstrated by downregulation of phosphorylated-IκBα, p-p65 and upregulation of IκBα, whilst miR-221 overexpression had an opposite result in ALI mice. Our findings demonstrate that inhibition of miR-221 can alleviate LPS-induced inflammation via inactivation of SOCS1/NF-κB signaling pathway in ALI mice.
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