ArticleCell death & disease2019
Abnormal inhibition of osteoclastogenesis by mesenchymal stem cells through the miR-4284/CXCL5 axis in ankylosing spondylitis.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Clinical significance and regulatory mechanism of miR-4284 in lumbar intervertebral disc degeneration.Journal of orthopaedic surgery and research · 2026Article
- Human peripheral osteoclast-precursor-development patterns reveal the significance of RPS17-dependent ribosome synthesis to Ankylosing Spondylitis lesions.Bone research · 2025Article
- Inhibition of miR-4284 could reduce apoptosis and neuroinflammation by targeting APBA1/JAK1/STAT3 signaling in Alzheimer's disease.Cell & bioscience · 2025Article
- Built-In Electric Field Accelerates Nanotopography-Mediated Enhancement of Vascularized Osseointegration via CaSmall science · 2025Article
- Targeting PTK2 by vaccarin alleviates osteoporosis through inhibiting ferroptosis via modulating P53 acetylation/succinylation.Cell biology and toxicology · 2025Article
- Clinical Progress in Mesenchymal Stem Cell Therapy: A Focus on Rheumatic Diseases.Immunity, inflammation and disease · 2025Review
- MGP regulates the adipogenic differentiation of mesenchymal stem cells in osteoporosis via the Ca2+/CaMKII/RIP140/FABP3 axis.Cell death discovery · 2025Article
- Fat mass and obesity-associated protein in mesenchymal stem cells inhibits osteoclastogenesisWorld journal of stem cells · 2025Article
- C-X-C motif chemokine ligand 13 suppresses osteoclast differentiation via interference with RANKL-RANK interaction.Frontiers in immunology · 2025Article
- Preparation and performance study ofRSC advances · 2024Article
- Nr4a1 enhances Wnt4 transcription to promote mesenchymal stem cell osteogenesis and alleviates inflammation-inhibited bone regeneration.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Nrf-2/ROS/NF-κB pathway is modulated by cynarin in human mesenchymal stem cells in vitro from ankylosing spondylitis.Clinical and translational science · 2024Article
- Chemokines in Cartilage Regeneration and Degradation: New Insights.International journal of molecular sciences · 2023Review
- Review
- The bone marrow side of axial spondyloarthritis.Nature reviews. Rheumatology · 2023Review
- USP7 promotes the osteoclast differentiation of CD14+ human peripheral blood monocytes in osteoporosis via HMGB1 deubiquitination.Journal of orthopaedic translation · 2023Article
- How Has Molecular Biology Enhanced Our Undertaking of axSpA and Its Management.Current rheumatology reports · 2023Review
- Transfer of microRNA-22-3p by M2 macrophage-derived extracellular vesicles facilitates the development of ankylosing spondylitis through the PER2-mediated Wnt/β-catenin axis.Cell death discovery · 2022Article
- Regulation of osteoclast-mediated bone resorption by microRNA.Cellular and molecular life sciences : CMLS · 2022Review
- [Hyperactivation of PI3K/AKT/mTOR signal pathway impairs TNF-α-induced autophagy in mesenchymal stem cells from patients with ankylosing spondylitis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ankylosing spondylitis (AS) is a common inflammatory autoimmune disease, characterized by pathological osteogenesis. Mesenchymal stem cells (MSCs), as the main source of osteoblasts, participate in bone remodeling not only through differentiation into osteoblasts but also through indirect regulation of osteoclastogenesis. Our previous study indicated that the stronger osteogenic differentiation of MSCs from AS patients (ASMSCs) involved in pathological osteogenesis. However, whether there is any abnormality in the regulation of osteoclastogenesis by ASMSCs remains unclear. In this study, ASMSCs or MSCs from healthy donors (HDMSCs) were co-cultured with CD14 + monocytes in osteoclast induction medium. Our results demonstrated that ASMSCs exhibited a stronger capacity to inhibit osteoclastogenesis than HDMSCs. To explore underlying mechanisms, cytokine array assays were performed, showing that ASMSCs secreted more CXCL5 than HDMSCs, which was confirmed by enzyme-linked immunosorbent assays. Moreover, inhibition of osteoclastogenesis by ASMSCs was recovered by decreasing CXCL5. Besides, the inhibitory effect of CXCL5 on osteoclastogenesis was confirmed by exogenous addition. Bioinformatics analysis was applied to find the interaction between miR-4284 and CXCL5, which was verified by luciferase reporter assays. Furthermore, we used miR-4284 inhibitors or mimics to prove that the expression of CXCL5 was regulated by miR-4284. Further analysis showed that downregulation of miR-4284 in MSCs resulted in increase of CXCL5, markedly inhibiting osteoclastogenesis, whereas upregulation of miR-4284 in MSCs had the opposite effect. Our findings indicate that ASMSCs exhibit a stronger capacity to inhibit osteoclastogenesis than HDMSCs through the miR-4284/CXCL5 axis, which provide a new perspective on the mechanism of pathologic osteogenesis in AS.
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