ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Peripheral TGF-β1 signaling is a critical event in bone cancer-induced hyperalgesia in rodents.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 77 citations in OpenAlex.
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- Cancer-nerve interplay in cancer progression and cancer-induced bone pain.Journal of bone and mineral metabolism · 2023Review
- Peripheral ablation of type III adenylyl cyclase induces hyperalgesia and eliminates KOR-mediated analgesia in mice.JCI insight · 2022Article
- Calcium Signalling in Breast Cancer Associated Bone Pain.International journal of molecular sciences · 2022Review
- TRPV1 in dorsal root ganglion contributed to bone cancer pain.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- Neurophysiological mechanisms of cancer-induced bone pain.Journal of advanced research · 2022Review
- Effect of TGF-Neural plasticity · 2022Article
- Physiological Changes and Pathological Pain Associated with Sedentary Lifestyle-Induced Body Systems Fat Accumulation and Their Modulation by Physical Exercise.International journal of environmental research and public health · 2021Review
- Development of Lipidoid Nanoparticles for siRNA Delivery to Neural Cells.The AAPS journal · 2021Article
- The Role of TGF-β in Bone Metastases.Biomolecules · 2021Review
- Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons.Neuroscience bulletin · 2021Article
- Oxidative stress induced by NOX2 contributes to neuropathic pain via plasma membrane translocation of PKCε in rat dorsal root ganglion neurons.Journal of neuroinflammation · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pain is the most common symptom of bone cancer. TGF-β, a major bone-derived growth factor, is largely released by osteoclast bone resorption during the progression of bone cancer and contributes to proliferation, angiogenesis, immunosuppression, invasion, and metastasis. Here, we further show that TGF-β1 is critical for bone cancer-induced pain sensitization. We found that, after the progression of bone cancer, TGF-β1 was highly expressed in tumor-bearing bone, and the expression of its receptors, TGFβRI and TGFβRII, was significantly increased in the DRG in a rat model of bone cancer pain that is based on intratibia inoculation of Walker 256 mammary gland carcinoma cells. The blockade of TGF-β receptors by the TGFβRI antagonist SD-208 robustly suppressed bone cancer-induced thermal hyperalgesia on post-tumor day 14 (PTD 14). Peripheral injection of TGF-β1 directly induced thermal hyperalgesia in intact rats and wide-type mice, but not in Trpv1(-/-) mice. Whole-cell patch-clamp recordings from DRG neurons showed that transient receptor potential vanilloid (TRPV1) sensitivity was significantly enhanced on PTD 14. Extracellular application of TGF-β1 significantly potentiated TRPV1 currents and increased [Ca(2+)]i in DRG neurons. Pharmacological studies revealed that the TGF-β1 sensitization of TRPV1 and the induction of thermal hyperalgesia required the TGF-βR-mediated Smad-independent PKCε and TGF-β activating kinase 1-p38 pathways. These findings suggest that TGF-β1 signaling contributes to bone cancer pain via the upregulation and sensitization of TRPV1 in primary sensory neurons and that therapeutic targeting of TGF-β1 may ameliorate the bone cancer pain in advanced cancer.
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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.