ArticleMolecular pain2014
PAR2-mediated upregulation of BDNF contributes to central sensitization in bone cancer pain.
Article in Molecular pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 59 citations in OpenAlex.
- Tetrahydropalmatine has analgesic role in mouse model of bone cancer pain by inactivating the TNF-α/uPA/PAR2/TRPV1 pathway in dorsal root ganglia.Cancer cell international · 2025Article
- Truncated TrkB: The predominant TrkB isoform in nociceptors.The journal of pain · 2025Article
- BDNF Signaling and Pain Modulation.Cells · 2025Review
- Brain-Derived Neurotrophic Factor, Nociception, and Pain.Biomolecules · 2024Review
- TIM-3 regulates the proliferation by BDNF-mediated PI3K/AKT axis in the process of endometriosis.Molecular medicine (Cambridge, Mass.) · 2023Article
- BDNF and its signaling in cancer.Journal of cancer research and clinical oncology · 2023Review
- Article
- The related mechanism of complete Freund's adjuvant-induced chronic inflammation pain based on metabolomics analysis.Biomedical chromatography : BMC · 2021Article
- Spinal PAR2 Activation Contributes to Hypersensitivity Induced by Peripheral Inflammation in Rats.International journal of molecular sciences · 2021Article
- Interplay of BDNF and GDNF in the Mature Spinal Somatosensory System and Its Potential Therapeutic Relevance.Current neuropharmacology · 2021Review
- Electroacupuncture Modulates Spinal BDNF/TrκB Signaling Pathway and Ameliorates the Sensitization of Dorsal Horn WDR Neurons in Spared Nerve Injury Rats.International journal of molecular sciences · 2020Article
- Effects of palmatine on BDNF/TrkB-mediated trigeminal neuralgia.Scientific reports · 2020Article
- Low-affinity neurotrophin receptor p75 of brain-derived neurotrophic factor contributes to cancer-induced bone pain by upregulating mTOR signaling.Experimental and therapeutic medicine · 2019Article
- Loss of STEP61 couples disinhibition to N-methyl-d-aspartate receptor potentiation in rodent and human spinal pain processing.Brain : a journal of neurology · 2019Article
- Protease activated receptor 2 (PAR2) activation causes migraine-like pain behaviors in mice.Cephalalgia : an international journal of headache · 2019Article
- The Somatostatin Receptor-4 Agonist J-2156 Alleviates Mechanical Hypersensitivity in a Rat Model of Breast Cancer Induced Bone Pain.Frontiers in pharmacology · 2018Article
- The mechanism of quercetin in regulating osteoclast activation and the PAR2/TRPV1 signaling pathway in the treatment of bone cancer pain.International journal of clinical and experimental pathology · 2018Article
- eIF4E Phosphorylation InfluencesFrontiers in cellular neuroscience · 2018Article
- EXPRESS: BDNF Signaling Contributes to Oral Cancer Pain in a Preclinical Orthotopic Rodent Model.Molecular pain · 2016Article
- Downregulation of miR-219 enhances brain-derived neurotrophic factor production in mouse dorsal root ganglia to mediate morphine analgesic tolerance by upregulating CaMKIIγ.Molecular pain · 2016Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBone cancer pain is currently a major clinical challenge for the management of cancer patients, and the cellular and molecular mechanisms underlying the spinal sensitization remain unclear. While several studies demonstrated the critical role of proteinase-activated receptor (PAR2) in the pathogenesis of several types of inflammatory or neuropathic pain, the involvement of spinal PAR2 and the pertinent signaling in the central sensitization is not determined yet in the rodent model of bone cancer pain.
findingsImplantation of tumor cells into the tibias induced significant thermal hyperalgesia and mechanical allodynia, and enhanced glutamatergic strength in the ipsilateral dorsal horn. Significantly increased brain-derived neurotrophic factor (BDNF) expression was detected in the dorsal horn, and blockade of spinal BDNF signaling attenuated the enhancement of glutamatergic strength, thermal hyperalgesia and mechanical allodynia in the rats with bone cancer pain. Significantly increased spinal PAR2 expression was also observed, and inhibition of PAR2 signaling ameliorated BDNF upsurge, enhanced glutamatergic strength, and thermal hyperalgesia and mechanical allodynia. Inhibition of NF-κB pathway, the downstream of PAR2 signaling, also significantly decreased the spinal BDNF expression, glutamatergic strength of dorsal horn neurons, and thermal hyperalgesia and mechanical allodynia.
conclusionThe present study demonstrated that activation of PAR2 triggered NF-κB signaling and significantly upregulated the BDNF function, which critically contributed to the enhancement of glutamatergic transmission in spinal dorsal horn and thermal and mechanical hypersensitivity in the rats with bone cancer. This indicated that PAR2 - NF-κB signaling might become a novel target for the treatment of pain in patients with bone cancer.
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