ArticleScientific reports2016
Activation of α2A-adrenergic signal transduction in chondrocytes promotes degenerative remodelling of temporomandibular joint.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Immuno-Mechanical Signaling Network Integration in Temporomandibular Joint Pathology: A TMID Conceptual Framework.International journal of molecular sciences · 2026Review
- Sensory and Sympathetic Nerve Localization in Mouse Temporomandibular Joint and Knee Joint Neuro-Musculoskeletal Tissues.Orthodontics & craniofacial research · 2025Article
- Autonomic Nervous System in Bone Remodeling: From Mechanisms to Novel Therapies in Orthopedic Diseases.Orthopaedic surgery · 2025Review
- Viral infections of the central nervous system increase the risk of knee osteoarthritis: a two-sample mendelian randomization study.Aging clinical and experimental research · 2025Article
- The function of GPCRs in different bone cells.International journal of biological sciences · 2025Review
- Sinomenine in cerebral ischemia: mechanisms, delivery strategies, and the emerging multifunctional biomaterials of the bone-brain axis.Frontiers in medicine · 2025Review
- Upregulated Mitochondrial Dynamics Is Responsible for the Procatabolic Changes of Chondrocyte Induced by α2-Adrenergic Signal Activation.Cartilage · 2024Article
- Equine Models of Temporomandibular Joint Osteoarthritis: A Review of Feasibility, Biomarkers, and Molecular Signaling.Biomedicines · 2024Review
- Critical signaling molecules in the temporomandibular joint osteoarthritis under different magnitudes of mechanical stimulation.Frontiers in pharmacology · 2024Review
- Patellar malalignment correlates with increased pain and increased synovial stress hormone levels-A cross-sectional study.PloS one · 2023Article
- The degeneration-pain relationship in the temporomandibular joint: Current understandings and rodent models.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Temporomandibular Joint Osteoarthritis: Pathogenic Mechanisms Involving the Cartilage and Subchondral Bone, and Potential Therapeutic Strategies for Joint Regeneration.International journal of molecular sciences · 2022Review
- Correlation between Adrenoceptor Expression and Clinical Parameters in Degenerated Lumbar Intervertebral Discs.International journal of molecular sciences · 2022Article
- Interaction of Neurovascular Signals in the Degraded Condylar Cartilage.Frontiers in bioengineering and biotechnology · 2022Article
- Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint.Journal of cellular and molecular medicine · 2021Review
- Yohimbine Ameliorates Temporomandibular Joint Chondrocyte Inflammation with Suppression of NF-κB Pathway.Inflammation · 2021Article
- β2-Adrenoceptor Deficiency Results in Increased Calcified Cartilage Thickness and Subchondral Bone Remodeling in Murine Experimental Osteoarthritis.Frontiers in immunology · 2021Article
- Driving βFrontiers in immunology · 2021Article
- G Protein-Coupled Receptors in Osteoarthritis.Frontiers in endocrinology · 2021Review
- Adrenoceptor Expression during Intervertebral Disc Degeneration.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study tested whether activation of adrenoreceptors in chondrocytes has roles in degenerative remodelling of temporomandibular joint (TMJ) and to determine associated mechanisms. Unilateral anterior crossbite (UAC) was established to induce TMJ degeneration in rats. Saline vehicle, α2- and β-adrenoreceptor antagonists or agonists were injected locally into the TMJ area of UAC rats. Cartilage degeneration, subchondral bone microarchitecture and the expression of adrenoreceptors, aggrecans, matrix metalloproteinases (MMPs) and RANKL by chondrocytes were evaluated. Chondrocytes were stimulated by norepinephrine to investigate signal transduction of adrenoreceptors. Increased α2A-adrenoreceptor expression was observed in condylar cartilage of UAC rats, together with cartilage degeneration and subchondral bone loss. Norepinephrine depresses aggrecans expression but stimulates MMP-3, MMP-13 and RANKL production by chondrocytes through ERK1/2 and PKA pathway; these effects were abolished by an α2A-adrenoreceptor antagonist. Furthermore, inhibition of α2A-adrenoreceptor attenuated degenerative remodelling in the condylar cartilage and subchondral bone, as revealed by increased cartilage thickness, proteoglycans and aggrecan expression, and decreased MMP-3, MMP-13 and RANKL expressions in cartilage, increased BMD, BV/TV, and decreased Tb.Sp in subchondral bone. Conversely, activation of α2A-adrenoreceptor intensified aforementioned degenerative changes in UAC rats. It is concluded that activation of α2A-adrenergic signal in chondrocytes promotes TMJ degenerative remodelling by chondrocyte-mediated pro-catabolic activities.
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Registered trials
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