ArticleBone & joint research2022
Long noncoding RNA H19 alleviates inflammation in osteoarthritis through interactions between TP53, IL-38, and IL-36 receptor.
Article in Bone & joint research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 36 citations in OpenAlex.
- Emerging roles of long non-coding RNAs in osteoarthritis: from molecular mechanisms to therapeutic opportunities.RNA biology · 2025Review
- Exploring the potential mechanisms of acetyl tributyl citrate exposure on osteoarthritis based on novel network toxicology.Scientific reports · 2025Article
- Identification of Genes Linked to Meniscal Degeneration in Osteoarthritis: An In Silico Analysis.International journal of molecular sciences · 2025Article
- LncRNA AC005165.1 Alleviates IL-1β-Induced Osteoarthritis via miR-199a-3p/TXNIP Axis.Biochemical genetics · 2025Article
- Mechanosensitive lncRNA H19 promotes chondrocyte autophagy, but not pyroptosis, by targeting miR-148a in post-traumatic osteoarthritis.Non-coding RNA research · 2025Article
- Article
- Role of IL-1 Family Cytokines IL-36, IL-37, IL-38 in Osteoarthritis and Rheumatoid Arthritis: A Comprehensive Review.Journal of inflammation research · 2024Review
- Bioinformatics and system biology analysis revealed the crosstalk between COVID-19 and osteoarthritis.Immunity, inflammation and disease · 2023Article
- Identification and verification of ferroptosis-related genes in diabetic foot using bioinformatics analysis.International wound journal · 2023Article
- Bioinformatics identification and integrative analysis of ferroptosis-related key lncRNAs in patients with osteoarthritis.Bioscience reports · 2023Article
- [Identification of Characteristic lncRNA Molecular Markers in Osteoarthritis by Integrating GEO Database and Machine Learning Strategies and Experimental Validation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Article
- Osteoarthritis related epigenetic variations in miRNA expression and DNA methylation.BMC medical genomics · 2023Article
- Role of Interleukin-36 in inflammatory joint diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023Review
- Article
- The emerging role of lncRNAs in osteoarthritis development and potential therapy.Frontiers in genetics · 2023Review
- Emerging role of lncRNAs in osteoarthritis: An updated review.Frontiers in immunology · 2022Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsOsteoarthritis (OA) is a common degenerative joint disease characterized by chronic inflammatory articular cartilage degradation. Long noncoding RNAs (lncRNAs) have been previously indicated to play an important role in inflammation-related diseases. Herein, the current study set out to explore the involvement of lncRNA H19 in OA.
methodsFirstly, OA mouse models and interleukin (IL)-1β-induced mouse chondrocytes were established. Expression patterns of IL-38 were determined in the synovial fluid and cartilage tissues from OA patients. Furthermore, the targeting relationship between lncRNA H19, tumour protein p53 (TP53), and IL-38 was determined by means of dual-luciferase reporter gene, chromatin immunoprecipitation, and RNA immunoprecipitation assays. Subsequent to gain- and loss-of-function assays, the levels of cartilage damage and proinflammatory factors were further detected using safranin O-fast green staining and enzyme-linked immunosorbent assay (ELISA) in vivo, respectively, while chondrocyte apoptosis was measured using Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) in vitro.
resultsIL-38 was highly expressed in lentivirus vector-mediated OA mice. Meanwhile, injection of exogenous IL-38 to OA mice alleviated the cartilage damage, and reduced the levels of proinflammatory factors and chondrocyte apoptosis. TP53 was responsible for lncRNA H19-mediated upregulation of IL-38. Furthermore, it was found that the anti-inflammatory effects of IL-38 were achieved by its binding with the IL-36 receptor (IL-36R). Overexpression of H19 reduced the expression of inflammatory factors and chondrocyte apoptosis, which was abrogated by knockdown of IL-38 or TP53.
conclusionCollectively, our findings evidenced that upregulation of lncRNA H19 attenuates inflammation and ameliorates cartilage damage and chondrocyte apoptosis in OA by upregulating TP53, IL-38, and by activating IL-36R.Cite this article:
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