ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Nociceptor beta II, delta, and epsilon isoforms of PKC differentially mediate paclitaxel-induced spontaneous and evoked pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 71 citations in OpenAlex.
- Article
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- Riluzole, a neuroprotective agent, preserves erectile function following bilateral cavernous nerve injury in male rats.International journal of impotence research · 2024Article
- Modified Akuamma Alkaloids with Increased Potency at the Mu-opioid Receptor.Journal of medicinal chemistry · 2023Article
- Calceolarioside A, a Phenylpropanoid Glycoside fromMolecules (Basel, Switzerland) · 2022Article
- Plasma Metabolomics and Lipidomics Differentiate Obese Individuals by Peripheral Neuropathy Status.The Journal of clinical endocrinology and metabolism · 2022Observational
- PKCζ-Mitogen-Activated Protein Kinase Signaling Mediates Crotalphine-Induced Antinociception.Toxins · 2021Article
- Activation of PKCε-ALDH2 Axis Prevents 4-HNE-Induced Pain in Mice.Biomolecules · 2021Article
- Corydalis saxicola Bunting total alkaloids attenuate paclitaxel-induced peripheral neuropathy through PKCε/p38 MAPK/TRPV1 signaling pathway.Chinese medicine · 2021Article
- Pharmacological rescue of cognitive function in a mouse model of chemobrain.Molecular neurodegeneration · 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
- The Calcium Channel α2δ1 Subunit: Interactional Targets in Primary Sensory Neurons and Role in Neuropathic Pain.Frontiers in cellular neuroscience · 2021Review
- Gabapentin and Duloxetine Prevent Oxaliplatin- and Paclitaxel-Induced Peripheral Neuropathy by Inhibiting Extracellular Signal-Regulated Kinase 1/2 (ERK1/2) Phosphorylation in Spinal Cords of Mice.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Regulation of the firing activity by PKA-PKC-Src family kinases in cultured neurons of hypothalamic arcuate nucleus.Journal of neuroscience research · 2020Article
- Pathogenesis of paclitaxel-induced peripheral neuropathy: A current review of in vitro and in vivo findings using rodent and human model systems.Experimental neurology · 2020Review
- Spinal and afferent PKC signaling mechanisms that mediate chronic pain in sickle cell disease.Neuroscience letters · 2019Review
- Activating transcription factor 3 modulates protein kinase C epsilon activation in diabetic peripheral neuropathy.Journal of pain research · 2019Article
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2 authors at 1 institution in 1 country.
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Abstract
As one of the most effective and frequently used chemotherapeutic agents, paclitaxel produces peripheral neuropathy (paclitaxel-induced peripheral neuropathy or PIPN) that negatively affects chemotherapy and persists after cancer therapy. The mechanisms underlying this dose-limiting side effect remain to be fully elucidated. This study aimed to investigate the role of nociceptor protein kinase C (PKC) isoforms in PIPN. Employing multiple complementary approaches, we have identified a subset of PKC isoforms, namely βII, δ, and ϵ, were activated by paclitaxel in the isolated primary afferent sensory neurons. Persistent activation of PKCβII, PKCδ, and PKCϵ was also observed in the dorsal root ganglion neurons after chronic treatment with paclitaxel in a mouse model of PIPN. Isoform-selective inhibitors of PKCβII, PKCδ, and PKCϵ given intrathecally dose-dependently attenuated paclitaxel-induced mechanical allodynia and heat hyperalgesia. Surprisingly, spinal inhibition of PKCβII and PKCδ, but not PKCϵ, blocked the spontaneous pain induced by paclitaxel. These data suggest that a subset of nociceptor PKC isoforms differentially contribute to spontaneous and evoked pain in PIPN, although it is not clear whether PKCϵ in other regions regulates spontaneous pain in PIPN. The findings can potentially offer new selective targets for pharmacological intervention of PIPN.
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