ArticleScientific reports2019
Degrading products of chondroitin sulfate can induce hypertrophy-like changes and MMP-13/ADAMTS5 production in chondrocytes.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- The regulatory significance of chondrocyte hypertrophy in maintaining chondrocyte homeostasis, regeneration and repair.Future science OA · 2026Review
- Proteoglycan Dynamics and Bone Quality: Molecular Regulation to Age-Related Fragility.Biomolecules · 2026Review
- Molecular Mechanisms of Chondrocyte Hypertrophy Mediated by Physical Cues and Therapeutic Strategies in Osteoarthritis.International journal of molecular sciences · 2026Review
- Sulfated Glycosaminoglycans in Inflammation.Advances in experimental medicine and biology · 2026Review
- A Multidimensional Definition of Pre-Osteoarthritis: Toward 21st-Century Subclinical Detection and Targeted Intervention.International journal of molecular sciences · 2025Review
- Article
- Integrase-Deficient Lentiviral Vector as a Platform for Efficient CRISPR/Cas9-Mediated Gene Editing for Mucopolysaccharidosis IVA.International journal of molecular sciences · 2025Article
- Cartilage-SpecificBiomedicines · 2025Article
- Senile Osteoarthritis Regulated by the Gut Microbiota: From Mechanisms to Treatments.International journal of molecular sciences · 2025Review
- Advancing Nanomedicine: For Bone Defect Repair and Regeneration.International journal of nanomedicine · 2025Review
- Catabolic mediators from TLR2-mediated proteoglycan aggrecan peptide-stimulated chondrocytes are reduced by Lactobacillus-conditioned media.Scientific reports · 2024Article
- Platelet-rich plasma alleviates knee arthritis in rats by inhibiting p65.Cell and tissue banking · 2024Article
- Arthritis and Duchenne muscular dystrophy: the role of chondroitin sulfate and its associated proteoglycans in disease pathology and as a diagnostic marker.American journal of physiology. Cell physiology · 2023Review
- Inhibition of NADPH Oxidases Prevents the Development of Osteoarthritis.Antioxidants (Basel, Switzerland) · 2022Article
- A bovine nucleus pulposus explant culture model.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022Article
- Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage.Cellular & molecular biology letters · 2022Article
- Article
- Microarray Analysis of Differential Gene Expression Between Traumatic Temporomandibular Joint Fibrous and Bony Ankylosis in a Sheep Model.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Dexamethasone-loaded thermo-sensitive hydrogel attenuates osteoarthritis by protecting cartilage and providing effective pain relief.Annals of translational medicine · 2021Article
- Nanoparticle-Cartilage Interaction: Pathology-Based Intra-articular Drug Delivery for Osteoarthritis Therapy.Nano-micro letters · 2021Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chondroitin sulfate (CS) is the most abundant glycosaminoglycan (GAG) in articular cartilage and the loss of CS-GAG occurs early in OA. As a major component of perichondral matrix interacting directly with chondrocytes, the active turnover of CS can affect to break the homeostasis of chondrocytes. Here we employ CS-based 3-dimensional (3D) hydrogel scaffold system to investigate how the degradation products of CS affect the catabolic phenotype of chondrocytes. The breakdown of CS-based ECM by the chondroitinase ABC (ChABC) resulted in a hypertrophy-like morphologic change in chondrocytes, which was accompanied by catabolic phenotypes, including increased MMP-13 and ADAMTS5 expression, nitric oxide (NO) production and oxidative stress. The inhibition of Toll-like receptor 2 (TLR2) or TLR4 with OxPAPC (TLR2 and TLR4 dual inhibitor) and LPS-RS (TLR4-MD2 inhibitor) ameliorated these catabolic phenotypes of chondrocytes by CS-ECM degradation, suggesting a role of CS breakdown products as damage-associated molecular patterns (DAMPs). As downstream signals of TLRs, MAP kinases, NF-kB, NO and STAT3-related signals were responsible for the catabolic phenotypes of chondrocytes associated with ECM degradation. NO in turn reinforced the activation of MAP kinases as well as NFkB signaling pathway. Thus, these results propose that the breakdown product of CS-GAG can recapitulate the catabolic phenotypes of OA.
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