ArticleMolecular pain2012
Dose-dependent expression of neuronal injury markers during experimental osteoarthritis induced by monoiodoacetate in the rat.
Article in Molecular pain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed.
- Activating Transcription Factor 3 in Pain: A Molecular Regulator and Emerging Biomarker.Genes · 2026Review
- Rheumatic diseases and metabolism: where centre and periphery meet.Nature reviews. Rheumatology · 2024Review
- Neural and immune roles in osteoarthritis pain: Mechanisms and intervention strategies.Journal of orthopaedic translation · 2024Review
- Platelet-rich plasma alleviates neuropathic pain in osteoarthritis by downregulating microglial activation.BMC musculoskeletal disorders · 2024Article
- Skeletal interoception in osteoarthritis.Bone research · 2024Review
- Review
- Assessment of the Impact of Physical Activity on the Musculoskeletal System in Early Degenerative Knee Joint Lesions in an Animal Model.International journal of molecular sciences · 2023Article
- Chronic pain and local pain in usually painless conditions including neuroma may be due to compressive proximal neural lesion.Frontiers in pain research (Lausanne, Switzerland) · 2023Article
- Translational evaluation of gait behavior in rodent models of arthritic disorders with the CatWalk device - a narrative review.Frontiers in medicine · 2023Review
- Osteoarthritis Pain in Old Mice Aggravates Neuroinflammation and Frailty: The Positive Effect of Morphine Treatment.Biomedicines · 2022Article
- Intra-articular injection of monoiodoacetate induces diverse hip osteoarthritis in rats, depending on its dose.BMC musculoskeletal disorders · 2022Article
- Article
- Joint Damage and Neuropathic Pain in Rats Treated With Lysophosphatidic Acid.Frontiers in immunology · 2022Article
- Article
- Dorsal Root Ganglia Macrophages Maintain Osteoarthritis Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Galactomannan of Delonix regia seeds reduces nociception and morphological damage in the rat model of osteoarthritis induced by sodium monoiodoacetate.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- TLR4 Antagonism Reduces Movement-Induced Nociception and ATF-3 Expression in Experimental Osteoarthritis.Journal of pain research · 2021Article
- Article
- Article
- Attenuation of the Diffuse Noxious Inhibitory Controls in Chronic Joint Inflammatory Pain Is Accompanied by Anxiodepressive-Like Behaviors and Impairment of the Descending Noradrenergic Modulation.International journal of molecular sciences · 2020Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIt was recently reported that the mono-iodoacetate (MIA) experimental model of osteoarthritis (OA) courses with changes of neurons innervating the affected joints that are commonly interpreted as a neuronal response to axonal injury. To better characterize these changes, we evaluated the expression of two markers of neuronal damage, ATF-3 and NPY, and the growth associated protein GAP-43, in primary afferent neurons of OA animals injected with three different doses of MIA (0.3, 1 or 2 mg). Measurements were performed at days 3, 7, 14, 21 and 31 post-MIA injection.
resultsOA animals showed the characteristic histopathological changes of the joints and the accompanying nociceptive behaviour, evaluated by the Knee-Bed and CatWalk tests. An increase of ATF-3 expression was detected in the DRG of OA animals as early as 3 days after the injection of 1 or 2 mg of MIA and 7 days after the injection of 0.3 mg. NPY expression was increased in animals injected with 1 or 2 mg of MIA, at day 3 or in all time-points, respectively. From day 7 onwards there was a massive increase of GAP-43 expression in ATF-3 cells.
conclusionsThe expression of the neuronal injury markers ATF-3 and NPY as well as an up-regulation of GAP-43 expression, indicative of peripheral fibre regeneration, suggests that axonal injury and a regeneration response may be happening in this model of OA. This opens new perspectives in the unravelling of the physiopathology of the human disease.
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