ArticleExperimental & molecular medicine2015
miR-139 modulates MCPIP1/IL-6 expression and induces apoptosis in human OA chondrocytes.
Article in Experimental & molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- The Role of Regnase-1 in Autoimmune Diseases - A Future Therapeutic Target for Clinical Use.Clinical reviews in allergy & immunology · 2026Review
- Inflammaging and osteoarthritis - therapeutic opportunities.Frontiers in immunology · 2026Review
- Targeted S100A8 PP-Cas9@PLGA-apt microparticles reduced cartilage degradation and subchondral bone isomerism in osteoarthritis treatment through JAK/STAT3 pathway modulation.Materials today. Bio · 2025Article
- Identification and characterisation of temporal abundance of microRNAs in synovial fluid from an experimental equine model of osteoarthritis.Equine veterinary journal · 2025Article
- Intraarticular treatment with integrin α10β1-selected mesenchymal stem cells affects microRNA expression in experimental post-traumatic osteoarthritis in horses.Frontiers in veterinary science · 2024Article
- Upregulating miR-181b promotes ferroptosis in osteoarthritic chondrocytes by inhibiting SLC7A11.BMC musculoskeletal disorders · 2023Article
- The role of apoptosis in the pathogenesis of osteoarthritis.International orthopaedics · 2023Review
- Identification of key genes and small molecule drugs in osteoarthritis by integrated bioinformatics analysis.Biochemistry and biophysics reports · 2023Article
- miR‑654‑5p inhibits autophagy by targeting ATG7 via mTOR signaling in intervertebral disc degeneration.Molecular medicine reports · 2021Article
- Review
- Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis.Frontiers in cell and developmental biology · 2021Review
- Exosomes Derived from M2 Macrophages Exert a Therapeutic Effect via Inhibition of the PI3K/AKT/mTOR Pathway in Rats with Knee Osteoarthritic.BioMed research international · 2021Article
- MCPIP-1 Restricts Inflammation via Promoting Apoptosis of Neutrophils.Frontiers in immunology · 2021Article
- Exosomal miRNAs in osteoarthritis.Molecular biology reports · 2020Review
- Epigenetics in osteoarthritis: Novel spotlight.Journal of cellular physiology · 2019Review
- Article
- The complex landscape of microRNAs in articular cartilage: biology, pathology, and therapeutic targets.JCI insight · 2018Review
- Onset and Progression of Human Osteoarthritis-Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?International journal of molecular sciences · 2018Review
- The Involvement of MicroRNAs in Osteoarthritis and Recent Developments: A Narrative Review.Mediterranean journal of rheumatology · 2018Review
- Inhibition of miR-126 protects chondrocytes from IL-1β induced inflammation via upregulation of Bcl-2.Bone & joint research · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
IL-6 is an inflammatory cytokine and its overexpression plays an important role in osteoarthritis (OA) pathogenesis. Expression of IL-6 is regulated post-transcriptionally by MCPIP1. The 3' untranslated region (UTR) of MCPIP1 mRNA harbors a miR-139 'seed sequence', therefore we examined the post-transcriptional regulation of MCPIP1 by miR-139 and its impact on IL-6 expression in OA chondrocytes. Expression of miR-139 was found to be high in the damaged portion of the OA cartilage compared with unaffected cartilage from the same patient and was also induced by IL-1β in OA chondrocytes. Inhibition of miR-139 decreased the expression of IL-6 mRNA by 38% and of secreted IL-6 protein by 40%. However, overexpression of miR-139 increased the expression of IL-6 mRNA by 36% and of secreted IL-6 protein by 56%. These data correlated with altered expression profile of MCPIP1 in transfected chondrocytes. Studies with a luciferase reporter construct confirmed the interactions of miR-139 with the 'seed sequence' located in the 3' UTR of MCPIP mRNA. Furthermore, miR-139 overexpression increased the catabolic gene expression but expression of anabolic markers remained unchanged. Overexpression of miR-139 also induced apoptosis in OA chondrocytes. Importantly, we also discovered that IL-6 is a potent inducer of miR-139 expression in OA chondrocytes. These findings indicate that miR-139 functions as a post-transcriptional regulator of MCPIP1 expression and enhances IL-6 expression, which further upregulates miR-139 expression in OA chondrocytes. These results support our hypothesis that miR-139-mediated downregulation of MCPIP1 promotes IL-6 expression in OA. Therefore, targeting miR-139 could be therapeutically beneficial in the management of OA.
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