ArticleJournal of orthopaedic surgery and research2022
microRNA-4701-5p protects against interleukin-1β induced human chondrocyte CHON-001 cells injury via modulating HMGA1.
Article in Journal of orthopaedic surgery and research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Elevated miR-409-5p may promote the progression of osteoarthritis by targeting DLST as a potential biomarker function of miR-409-5p in osteoarthritis.Journal of orthopaedic surgery and research · 2026Article
- HMGA1 Regulates IRS2 to Promote Inflammatory Responses and Oxidative Stress Injury in MPPCell biochemistry and biophysics · 2025Article
- Expression of miR-92a in Green Tea EGCG Preconditioned Adiposederived Stem Cells Ameliorates Inflammatory Response and Increases Cartilage Regeneration in RA Rats through KLF4/IL-17/MMP-2 Axis Modulation.Current gene therapy · 2025Article
- Current status and future prospects of nanocarrier-mediated miRNA delivery for osteoarthritis therapy.Frontiers in medicine · 2025Review
- MiR-98-5p plays suppressive effects on IL-1β-induced chondrocyte injury associated with osteoarthritis by targeting CASP3.Journal of orthopaedic surgery and research · 2024Article
- The role of apoptosis in the pathogenesis of osteoarthritis.International orthopaedics · 2023Review
- LncRNA HAGLR silencing inhibits IL-1β-induced chondrocytes inflammatory injury via miR-130a-3p/JAK1 axis.Journal of orthopaedic surgery and research · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundmiRNA-4701-5p has been reported to be a vital regulator in many diseases, including rheumatoid arthritis, and miRNA-4701-5p is evidenced to be participated in synovial invasion and joint destruction. In our report, we investigated the roles of miRNA-4701-5p in osteoarthritis (OA) and analyzed the molecular mechanism.
methodsInterleukin-1β (IL-1β) was applied for stimulating human chondrocyte CHON-001 cells to establish an OA injury model. mRNA levels and protein expression were measured using qRT-PCR and western blot assay, respectively. The proliferation ability and cytotoxicity of CHON-001 cells were checked using MTT assay and lactate dehydrogenase activity. The inflammation of chondrocytes was accessed by the secretion levels of interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor (TNF)-α. The apoptosis of chondrocytes was determined by flow cytometry assay. Bioinformatics software Starbase v2.0 analyzed the functional binding sites between miRNA-4701-5p and HMGA1 and the interaction was further confirmed using dual luciferase reporter analysis.
resultsmiRNA-4701-5p was down-regulated in the IL-1β-stimulated chondrocytes and HMGA1 directly targeted miRNA-4701-5p. Up-regulation of miRNA-4701-5p could alleviate IL-1β-treated CHON-001 cells inflammation and apoptosis, and reversed the cell proliferation decrease and cytotoxicity increase after IL-1β treatment. Nevertheless, all the roles of miRNA-4701-5p overexpression in CHON-001 cells could be reversed by HMGA1 up-regulation.
conclusionsmiRNA-4701-5p could alleviate the inflammatory injury of IL-1β-treated CHON-001 cells via down-regulating HMGA1, indicating that miRNA-4701-5p/HMGA1 is a promising therapeutic target for OA.
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