ArticleAnnals of biomedical engineering2016
Spinal Astrocytic Thrombospondin-4 Induced by Excitatory Neuronal Signaling Mediates Pain After Facet Capsule Injury.
Article in Annals of biomedical engineering, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Subfailure capsule strain as the cause of cervical zygapophysial joint pain after whiplash: a scoping review.Pain medicine (Malden, Mass.) · 2026Article
- Multifaceted Astrocyte-Neuron Cross-Talk in Neuropathic Pain: Potential Mechanisms and Functional Implications.Journal of pain research · 2026Review
- Expression of thrombospondin-4 in the infrapatellar fat pad and synovial fluid - potential contribution to osteoarthritis pain.Arthritis research & therapy · 2025Article
- Toward discovering a novel family of peptides targeting neuroinflammatory states of brain microglia and astrocytes.Journal of neurochemistry · 2024Article
- Pathophysiological roles of thrombospondin-4 in disease development.Seminars in cell & developmental biology · 2024Review
- 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
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Thrombospondin-4 (TSP4) is a synaptogenic molecule that is upregulated in the spinal cord after painful facet joint injury and may contribute to spinal hyperexcitability. However, the mechanisms leading to increased spinal TSP4 are unclear. Because primary afferent activity is critical in the development of spinal hyperexcitability after facet joint injury, this study evaluated the role of afferent firing in the increase of spinal TSP4 and excitatory synapses. Intra-articular bupivacaine was administered immediately or 4 days after painful facet joint injury in male Holtzman rats, and TSP4 and excitatory synapses were quantified in the spinal cord at day 7. Immediate, but not delayed bupivacaine treatment, prevents the injury-induced increase in TSP4 and excitatory synapses in the dorsal horn (p < 0.0001). Preliminary in vitro experiments suggest that the excitatory signaling molecules ATP and glutamate may stimulate astrocytic TSP4 expression (p ≤ 0.04). Collectively, these results suggest that afferent activity early after facet joint injury is critical for the induction of spinal TSP4. This study advances the understanding of the timing and role of afferent activity in TSP4 expression after injury, which is critical for the therapeutic targeting of TSP4 to treat persistent pain conditions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.