ArticleBritish journal of pharmacology2016
Involvement of Rac1 signalling pathway in the development and maintenance of acute inflammatory pain induced by bee venom injection.
Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 35 citations in OpenAlex.
- Molecular Mediators of Neutrophil Primary Granule Release Following Acute Ischemic Stroke and their Associated Epigenetic Modulation by HDAC2.Molecular neurobiology · 2025Article
- Netrin-1 Promotes M2 Type Activation and Inhibits Pyroptosis of Microglial Cells by Depressing RAC1/Nf-?B Pathway to Alleviate Inflammatory Pain.Physiological research · 2024Article
- Study on the transcriptome for breast muscle of chickens and the function of key gene RAC2 on fibroblasts proliferation.BMC genomics · 2021Article
- Dendritic Spines in the Spinal Cord: Live Action Pain.Neuroscience insights · 2020Article
- Spinal cord motor neuron plasticity accompanies second-degree burn injury and chronic pain.Physiological reports · 2019Article
- Involvement of Rac1 signalling pathway in the development and maintenance of acute inflammatory pain induced by bee venom injection.British journal of pharmacology · 2016Article
- Therapeutic potential of Pak1 inhibition for pain associated with cutaneous burn injury.Molecular painArticle
- Rac1/PAK1 signaling contributes to bone cancer pain by Regulation dendritic spine remodeling in rats.Molecular painArticle
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe Rho GTPase, Rac1, is involved in the pathogenesis of neuropathic pain induced by malformation of dendritic spines in the spinal dorsal horn (sDH) neurons. In the present study, the contribution of spinal Rac1 to peripheral inflammatory pain was studied. EXPERIMENTAL APPROACH: Effects of s.c. bee venom (BV) injection on cellular localization of Rac1 in the rat sDH was determined with double labelling immunofluorescence. Activation of Rac1 and its downstream effector p21-activated kinase (PAK), ERKs and p38 MAPK in inflammatory pain states was evaluated with a pull-down assay and Western blotting. The preventive and therapeutic analgesic effects of intrathecal administration of NSC23766, a selective inhibitor of Rac1, on BV-induced spontaneous nociception and pain hypersensitivity were investigated. KEY
resultsRac1 labelling was mainly localized within neurons in both the superficial and deep layers of the sDH in rats of naïve, vehicle-treated and inflamed (BV injected) groups. GTP-Rac1-PAK and ERKs/p38 were activated following s.c. BV injection. Post-treatment with intrathecal NSC23766 significantly inhibited GTP-Rac1 activity and phosphorylation of Rac1-PAK, ERKs and p38 MAPK in the sDH. Both pre-treatment and post-treatment with intrathecal NSC23766 dose-dependently attenuated the paw flinches, primary thermal and mechanical hyperalgesia and the mirror-image thermal hyperalgesia induced by BV injection, but without affecting the baseline pain sensitivity and motor coordination. CONCLUSIONS AND IMPLICATIONS: The spinal GTP-Rac1-PAK-ERK/p38MAPK signalling pathway is involved in both the development and maintenance of peripheral inflammatory pain and can be used as a potential molecular target for developing a novel therapeutic strategy for clinical pain.
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