ArticleInflammation2020
microRNA-21 Aggravates Lipopolysaccharide-Induced Inflammation in MH7A Cells Through Targeting SNF5.
Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Role of the PI3K/AKT signaling pathway in regulating gene expression in rheumatoid arthritis (Review).Molecular medicine reports · 2026Review
- The role of miR-21 in early-stage lung adenocarcinoma: clinical and bioinformatics insights.Scientific reports · 2025Article
- RNA-seq Based Transcriptome Analysis Reveals Role of Myoglobin in Rheumatoid Arthritis.Inflammation · 2025Article
- Hsa-miR-21-5p is induced by interleukin-6 and affects multiple pathogenic factors associated with fibroblast-like synoviocytes in rheumatoid arthritis.Scientific reports · 2025Article
- PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024Review
- Role of miRNAs in Rheumatoid Arthritis Therapy.Cells · 2023Review
- Challenges and promise of targeting miRNA in rheumatic diseases: a computational approach to identify miRNA association with cell types, cytokines, and disease mechanisms.Frontiers in immunology · 2023Review
- The non-coding RNA interactome in joint health and disease.Nature reviews. Rheumatology · 2021Review
- Compounds DRG and DAG, Two Phenol Glycosides, Inhibit TNF-α-stimulated Inflammatory Response through Blocking NF-kB/AKT/JNK Signaling Pathways in MH7A Cells.Inflammation · 2021Article
- MicroRNA-489-3p plays a significant role in congenital hypothyroidism through regulating neuronal cell apoptosis via targeting translationally controlled tumor protein 1.Experimental and therapeutic medicine · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The research aims to explore the roles and underlying mechanisms of microRNA-21 (miR-21) in lipopolysaccharide (LPS)-induced inflammation in MH7A cells. Cells were treated with LPS and/or transfected with miR-21 mimic/inhibitor or pc-sucrose nonfermentable 5 (SNF5). Cell viability was detected by CCK-8. ELISA and western blot were respectively conducted to measure the protein levels of pro-inflammatory factors, NF-κB or PTEN/PI3K/AKT key proteins and SNF5. miR-21/U6 was measured by qRT-PCR. The association between miR-21 and SNF5 was determined by luciferase reporter assay. Cell viability and the protein expression levels of interleukin-1β (IL-1β), IL-6, and p/t-p65, p/t-IκBα, p/t-PI3K, and p/t-AKT were significantly elevated by LPS, but with an inhibition of p-PTEN. Besides, LPS upregulated miR-21, whose overproduction or silence enhanced or alleviated the LPS stimulation on those elements above, respectively. miR-21 mimic notably inhibited SNF5, which was accelerated by miR-21 inhibitor, and abundant SNF5 abolished the effect of miR-21 mimic on cell viability, pro-inflammatory mediators, and sensitivity of signaling pathways, representing a negative relationship between them. miR-21 augmented LPS-induced inflammation response through activating NF-κB and PTEN/PI3K/AKT pathways by silencing SNF5 in MH7A cell line.
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Registered trials
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