ArticleInternational journal of molecular sciences2022
Semaphorin 3A-Neuropilin-1 Signaling Modulates MMP13 Expression in Human Osteoarthritic Chondrocytes.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Neuropilin‑1: Emerging roles in nerve‑vessel‑bone coupling during fracture repair (Review).International journal of molecular medicine · 2026Review
- Plasma and Synovial Fluid VEGF-A and Neuropilin-1 in Knee Osteoarthritis: Associations With Radiographic Severity, Pain Sensitization-Related Features, and Disease Burden.The Kaohsiung journal of medical sciences · 2026Article
- Semaphorin3A Rewires CD4International journal of molecular sciences · 2025Article
- Peripheral neuronal sensitization and neurovascular remodelling in osteoarthritis pain.Nature reviews. Rheumatology · 2025Review
- Research progress on exosomes from different sources in osteoarthritis and cartilage injury.Journal of orthopaedic surgery and research · 2025Review
- Mechanisms and Therapeutic Strategies of Macrophage Polarization in Intervertebral Disc Degeneration.JOR spine · 2025Review
- Loss of SCRG1 in chondrocytes inhibits osteoarthritis by promoting autophagy activity in the temporomandibular joint through inhibition of neurokine receptors.Journal of oral & facial pain and headache · 2025Article
- An Update on Emerging Regenerative Medicine Applications: The Use of Extracellular Vesicles and Exosomes for the Management of Chronic Pain.Current pain and headache reports · 2024Review
- In focus in HCB.Histochemistry and cell biology · 2024Article
- The emerging role of the semaphorin family in cartilage and osteoarthritis.Histochemistry and cell biology · 2024Review
- Semaphorin 3 a restores the ability of type 1 regulatory T cells to suppress food allergy.Immunologic research · 2024Article
- Article
- Development and Degeneration of the Intervertebral Disc-Insights from Across Species.Veterinary sciences · 2023Review
- The effects of semaphorin 3A in bone and cartilage metabolism: fundamental mechanism and clinical potential.Frontiers in cell and developmental biology · 2023Review
- MicroRNA-15a/β1,4-GalT-I axis contributes to cartilage degeneration via NF-κB signaling in osteoarthritis.Clinics (Sao Paulo, Brazil) · 2023Article
- Overexpression of NRP1 is Associated with Poor Prognosis via Accelerating Immunosuppression in Head and Neck Squamous Cell Carcinoma.International journal of general medicine · 2023Article
- Proteomic profiling of extracellular vesicles in synovial fluid and plasma from Oligoarticular Juvenile Idiopathic Arthritis patients reveals novel immunopathogenic biomarkers.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Osteoarthritis (OA) is a complex disorder of diarthrodial joints caused by multiple risk factors and is characterized by articular cartilage destruction as well as changes in other articular tissues. Semaphorin 3A (Sema3A), known to be a chemo-repellent for sensory nerve fibers, has recently been implicated in cartilage OA pathophysiology. We demonstrated that the expression of SEMA3A and its receptor neuropilin-1 (NRP1) are synchronously upregulated in chondrocytes isolated from knee cartilage of OA patients compared to non-OA control chondrocytes. In addition, we observed that during in vitro passaging of OA chondrocytes, the Nrp-1 level increases, whereas the Sema3A level decreases. In this study, we aimed to uncover how Sema3A-Nrp-1 signaling affects metabolism and viability of OA chondrocytes via siRNA-mediated inhibition of Nrp-1 expression. We observed a decreased proliferation rate and an increase in adhesion and senescence after Nrp-1 silencing. Moreover, MMP13 gene expression was reduced by approximately 75% in NRP1 knockdown OA chondrocytes, whereas MMP13 expression was induced by Sema3A treatment in control (nt siRNA) OA chondrocytes, accompanied by an impaired AKT phosphorylation. These findings suggest a potential catabolic function of Sema3A signaling in OA chondrocytes by inducing MMP13 expression and by compromising pro-survival AKT activation. We propose that targeting the Sema3A-Nrp-1 signaling axis might be an opportunity to interfere with OA pathogenesis and progression.
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Registered trials
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