ArticleArthritis & rheumatology (Hoboken, N.J.)2015
MicroRNA-9 promotion of interleukin-6 expression by inhibiting monocyte chemoattractant protein-induced protein 1 expression in interleukin-1β-stimulated human chondrocytes.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 66 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
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- Epigenetic therapy targeting bone marrow mesenchymal stem cells for age-related bone diseases.Stem cell research & therapy · 2022Review
- Epigenetic Regulation of Chondrocytes and Subchondral Bone in Osteoarthritis.Life (Basel, Switzerland) · 2022Review
- Long non-coding ribonucleic acid AFAP1-AS1 promotes chondrocyte proliferation via the miR-512-3p/matrix metallopeptidase 13 (MMP-13) axis.Bioengineered · 2022Article
- Prediction and analysis of microRNAs involved in COVID-19 inflammatory processes associated with the NF-kB and JAK/STAT signaling pathways.International immunopharmacology · 2021Review
- Upregulated endonuclease Regnase-1 suppresses osteoarthritis by forming a negative feedback loop of catabolic signaling in chondrocytes.Arthritis research & therapy · 2021Article
- Expression of inflammatory interleukins and selected miRNAs in non-small cell lung cancer.Scientific reports · 2021Article
- Review
- Comprehensive Analysis of Key Genes, Signaling Pathways and miRNAs in Human Knee Osteoarthritis: Based on Bioinformatics.Frontiers in pharmacology · 2021Article
- MCPIP-1 Restricts Inflammation via Promoting Apoptosis of Neutrophils.Frontiers in immunology · 2021Article
- Lysosomal dysfunction in osteoarthritis and aged cartilage triggers apoptosis in chondrocytes through BAX mediated release of Cytochrome c.Osteoarthritis and cartilage · 2021Article
- Impacts of Green Tea on Joint and Skeletal Muscle Health: Prospects of Translational Nutrition.Antioxidants (Basel, Switzerland) · 2020Review
- Article
- Article
- Exosomal miRNAs in osteoarthritis.Molecular biology reports · 2020Review
- MiR-421 promotes the development of osteosarcoma by regulating MCPIP1 expression.Cancer biology & therapy · 2020Article
- Effect of oxidative stress and 3-hydroxytyrosol on DNA methylation levels of miR-9 promoters.Journal of cellular and molecular medicine · 2019Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveEnhanced expression of interleukin-6 (IL-6) plays an important role in the pathogenesis of osteoarthritis (OA). Monocyte chemoattractant protein-induced protein 1 (MCPIP-1) is a novel posttranscriptional regulator of IL-6 expression and is targeted by microRNA-9 (miR-9). We investigated the expression of MCPIP-1 in OA cartilage and explored whether targeting of MCPIP-1 by miR-9 contributes to enhanced IL-6 expression in OA.
methodsGene and protein expression in IL-1β-stimulated human OA chondrocytes/cartilage was determined by TaqMan assay and immunoblotting, respectively. Messenger RNA (mRNA) for MCPIP-1 and IL-6 expression at the single-cell level was analyzed using RNAscope. MCPIP-1 protein interaction with IL-6 mRNA was investigated using RNA immunoprecipitation. Transient transfections were used for the small interfering RNA (siRNA)-mediated knockdown and overexpression of MCPIP-1, its RNase-defective mutant miR-9, or antagomir. The role of signaling pathways was evaluated using small-molecule inhibitors. Binding of miR-9 with the "seed sequence" in the 3'-untranslated region of MCPIP-1 mRNA was investigated using a luciferase reporter assay.
resultsMCPIP-1 mRNA expression was low, but expression of miR-9 and IL-6 was high, in damaged OA cartilage. In IL-1β-stimulated OA chondrocytes, the expression of miR-9 and MCPIP-1 was mutually exclusive, and increased expression of miR-9 correlated with reduced MCPIP-1 expression and enhanced IL-6 expression. MCPIP-1 protein directly binds with IL-6 mRNA, and overexpression of wild-type MCPIP-1 destabilized the IL-6 mRNA. MCPIP-1 expression was altered by overexpression or inhibition of miR-9. Transfection with miR-9 mimics inhibited the reporter activity, and mutation of the "seed sequence" abolished the repression of reporter activity.
conclusionThese findings implicate miR-9-mediated suppression of MCPIP-1 in the pathogenesis of OA via up-regulation of IL-6 expression in IL-1β-stimulated human OA chondrocytes.
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