ArticleExperimental neurology2015
Thrombospondin-4 and excitatory synaptogenesis promote spinal sensitization after painful mechanical joint injury.
Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Subfailure capsule strain as the cause of cervical zygapophysial joint pain after whiplash: a scoping review.Pain medicine (Malden, Mass.) · 2026Article
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Expression of thrombospondin-4 in the infrapatellar fat pad and synovial fluid - potential contribution to osteoarthritis pain.Arthritis research & therapy · 2025Article
- The mechanobiology of extracellular matrix: a focus on thrombospondins.Cell communication and signaling : CCS · 2025Review
- The Burning Pain Transcriptome in the Mouse Primary Somatosensory Cortex.International journal of molecular sciences · 2025Article
- The Role of Thrombospondins in Osteoarthritis: from Molecular Mechanisms to Therapeutic Potential.International journal of biological sciences · 2025Review
- Human-induced pluripotent stem cell-derived neural stem/progenitor cell ex vivo gene therapy with synaptic organizer CPTX for spinal cord injury.Stem cell reports · 2024Article
- Pathophysiological roles of thrombospondin-4 in disease development.Seminars in cell & developmental biology · 2024Review
- Complement C3a treatment accelerates recovery after stroke via modulation of astrocyte reactivity and cortical connectivity.The Journal of clinical investigation · 2023Article
- Pregabalin for chemotherapy-induced neuropathy: background and rationale for further study.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2022Review
- Generation of Matrix Degradation Products Using an In Vitro MMP Cleavage Assay.International journal of molecular sciences · 2022Article
- Effects of cyanocobalamin and its combination with morphine on neuropathic rats and the relationship between these effects and thrombospondin-4 expression.The Korean journal of pain · 2022Article
- COMP and TSP-4: Functional Roles in Articular Cartilage and Relevance in Osteoarthritis.International journal of molecular sciences · 2021Article
- The Calcium Channel α2δ1 Subunit: Interactional Targets in Primary Sensory Neurons and Role in Neuropathic Pain.Frontiers in cellular neuroscience · 2021Review
- Intra-articular collagenase in the spinal facet joint induces pain, DRG neuron dysregulation and increased MMP-1 absent evidence of joint destruction.Scientific reports · 2020Article
- Effects of thrombospondin-4 on pro-inflammatory phenotype differentiation and apoptosis in macrophages.Cell death & disease · 2020Article
- Direct, gabapentin-insensitive interaction of a soluble form of the calcium channel subunit αScientific reports · 2019Article
- Thrombospondin-4 in tissue remodeling.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- COMP and TSP-4 interact specifically with the novel GXKGHR motif only found in fibrillar collagens.Scientific reports · 2018Article
- Pre-treatment with Meloxicam Prevents the Spinal Inflammation and Oxidative Stress in DRG Neurons that Accompany Painful Cervical Radiculopathy.Neuroscience · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Facet joint injury induces persistent pain that may be maintained by structural plasticity in the spinal cord. Astrocyte-derived thrombospondins, especially thrombospondin-4 (TSP4), have been implicated in synaptogenesis and spinal sensitization in neuropathic pain, but the TSP4 response and its relationship to synaptic changes in the spinal cord have not been investigated for painful joint injury. This study investigates the role of TSP4 in the development and maintenance of persistent pain following injurious facet joint distraction in rats and tests the hypothesis that excitatory synaptogenesis contributes to such pain. Painful facet joint loading induces dorsal horn excitatory synaptogenesis along with decreased TSP4 in the DRG and increased astrocytic release of TSP4 in the spinal cord, all of which parallel the time course of sustained tactile allodynia. Blocking injury-induced spinal TSP4 expression with antisense oligonucleotides or reducing TSP4 activity at its neuronal receptor in the spinal cord with gabapentin treatment both attenuate the allodynia and dorsal horn synaptogenesis that develop after painful facet joint loading. Increased spinal TSP4 also facilitates the development of allodynia and spinal hyperexcitability, even after non-painful physiological loading of the facet joint. These results suggest that spinal TSP4 plays an important role in the development and maintenance of persistent joint-mediated pain by inducing excitatory synaptogenesis and facilitating the transduction of mechanical loading of the facet joint that leads to spinal hyperexcitability.
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