ArticleActa pharmacologica Sinica2016
MicroRNA-124 negatively regulates LPS-induced TNF-α production in mouse macrophages by decreasing protein stability.
Article in Acta pharmacologica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Characterisation and Comparative Evaluation of miRNA Contained in Small Extracellular Vesicles Isolated From Bovine Milk and Whey.Journal of extracellular biology · 2026Article
- Deubiquitinase USP14 is upregulated in Crohn's disease and inhibits the NOD2 pathway mediated inflammatory responseEuropean journal of histochemistry : EJH · 2024Article
- High dietary Fructose Drives Metabolic Dysfunction-Associated Steatotic Liver Disease via Activating ubiquitin-specific peptidase 2/11β-hydroxysteroid dehydrogenase type 1 Pathway in Mice.International journal of biological sciences · 2024Article
- The role of the gut microbiome and its metabolites in cerebrovascular diseases.Frontiers in microbiology · 2023Review
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- Stem cell-derived extracellular vesicles reduce the expression of molecules involved in cardiac hypertrophy-In a model of human-induced pluripotent stem cell-derived cardiomyocytes.Frontiers in pharmacology · 2022Article
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- Role of Epigenetics in the Regulation of Immune Functions of the Skin.The Journal of investigative dermatology · 2021Review
- USP2-Related Cellular Signaling and Consequent Pathophysiological Outcomes.International journal of molecular sciences · 2021Review
- The Role of Deubiquitinases in Vascular Diseases.Journal of cardiovascular translational research · 2020Review
- The Proteasome and Its Network: Engineering for Adaptability.Cold Spring Harbor perspectives in biology · 2020Review
- MicroRNA124-IL6R Mediates the Effect of Nicotine in Inflammatory Bowel Disease by Shifting Th1/Th2 Balance Toward Th1.Frontiers in immunology · 2020Article
- miR-135a deficiency inhibits the AR42J cells damage in cerulein-induced acute pancreatitis through targeting FAM129A.Pflugers Archiv : European journal of physiology · 2019Article
- Inhibition of ubiquitin-specific protease 2 causes accumulation of reactive oxygen species, mitochondria dysfunction, and intracellular ATP decrement in C2C12 myoblasts.Physiological reports · 2019Article
- Both anti-inflammatory and antiviral properties of novel drug candidate ABX464 are mediated by modulation of RNA splicing.Scientific reports · 2019Article
- From Oxidative Stress Damage to Pathways, Networks, and Autophagy via MicroRNAs.Oxidative medicine and cellular longevity · 2018Article
- Article
- MicroRNAs associated with inflammation in shoulder tendinopathy and glenohumeral arthritis.Molecular and cellular biochemistry · 2018Article
- Anti-Inflammatory MicroRNAs and Their Potential for Inflammatory Diseases Treatment.Frontiers in immunology · 2018Review
- ICAM-1 regulates macrophage polarization by suppressing MCP-1 expression via miR-124 upregulation.Oncotarget · 2017Article
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9 authors.
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Abstract
aimMicroRNAs play pivotal roles in regulation of both innate and adaptive immune responses. In the present study, we investigated the effects of microRNA-124 (miR-124) on production of the pro-inflammatory cytokine TNF-α in lipopolysaccharide (LPS)-treated mouse macrophages.
methodsMouse macrophage cell line RAW264.7 was stimulated with LPS (100 ng/mL). The levels of miR-124 and TNF-α mRNA were evaluated using q-PCR. ELISA and Western blotting were used to detect TNF-α protein level in cell supernatants and cells, respectively. 3'-UTR luciferase reporter assays were used to analyze the targets of miR-124. For in vivo experiments, mice were injected with LPS (30 mg/kg, ip).
resultsLPS stimulation significantly increased the mRNA level of miR-124 in RAW264.7 macrophages in vitro and mice in vivo. In RAW264.7 macrophages, knockdown of miR-124 with miR-124 inhibitor dose-dependently increased LPS-stimulated production of TNF-α protein and prolonged the half-life of TNF-α protein, but did not change TNF-α mRNA levels, whereas overexpression of miR-124 with miR-124 mimic produced the opposite effects. Furthermore, miR-124 was found to directly target two components of deubiquitinating enzymes: ubiquitin-specific proteases (USP) 2 and 14. Knockdown of USP2 or USP14 accelerated protein degradation of TNF-α, and abolished the effect of miR-124 on TNF-α protein stability.
conclusionmiR-124, targeting USP2 and USP14, negatively regulates LPS-induced TNF-α production in mouse macrophages, suggesting miR-124 as a new therapeutic target in inflammation-related diseases.
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