ArticleAnesthesiology2011
Isozyme-specific effects of protein kinase C in pain modulation.
Article in Anesthesiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- An Update on Protein Kinases as Therapeutic Targets-Part I: Protein Kinase C Activation and Its Role in Cancer and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- GABACells · 2022Article
- Cross-Talk of Toll-Like Receptor 5 and Mu-Opioid Receptor Attenuates Chronic Constriction Injury-Induced Mechanical Hyperalgesia through a Protein Kinase C Alpha-Dependent Signaling.International journal of molecular sciences · 2021Article
- PKCγ interneurons, a gateway to pathological pain in the dorsal horn.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Spinal and afferent PKC signaling mechanisms that mediate chronic pain in sickle cell disease.Neuroscience letters · 2019Review
- 5-HTThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Spinal PKCα inhibition and gene-silencing for pain relief: AMPAR trafficking at the synapses between primary afferents and sensory interneurons.Scientific reports · 2018Article
- PKCβII-induced upregulation of PGP9.5 and VEGF in postoperative persistent pain in rats.Journal of pain research · 2018Article
- PKCδ-targeted intervention relieves chronic pain in a murine sickle cell disease model.The Journal of clinical investigation · 2016Article
- Epac-protein kinase C alpha signaling in purinergic P2X3R-mediated hyperalgesia after inflammation.Pain · 2016Article
- Phosphoinositide signaling in somatosensory neurons.Advances in biological regulation · 2016Review
- Intact subepidermal nerve fibers mediate mechanical hypersensitivity via the activation of protein kinase C gamma in spared nerve injury.Molecular pain · 2016Article
- Article
- Article
- Dorsal Horn Circuits for Persistent Mechanical Pain.Neuron · 2015Article
- Protein kinase Cδ mediates histamine-evoked itch and responses in pruriceptors.Molecular pain · 2015Article
- Article
- Early down-regulation of PKCδ as a pro-survival mechanism in Huntington's disease.Neuromolecular medicine · 2014Article
- PKCγ receptor mediates visceral nociception and hyperalgesia following exposure to PTSD-like stress in the spinal cord of rats.Molecular pain · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundProtein kinase C (PKC) is a family of serine/threonine kinases that contains more than 10 isozymes. Evidence suggests that PKC may play important roles in pain modulation, but the isozyme-specific effects of PKC on different aspects of pain modulation are not fully understood. We hypothesize that different PKC isozymes play different roles in different aspects of pain modulation.
methodsThe nociceptive behaviors of mice with deletion of PKCα, β, γ, or δ in multiple pain models were compared with their respective wild-type littermates. Also, morphine analgesia and the development of morphine tolerance in mice with deletion of PKCγ were compared with their respective wild-type littermates.
resultsThermal hyperalgesia induced by complete Freund's adjuvant injection was significantly attenuated by the deletion of PKCβ, γ, or δ, but not PKCα. Deletion of PKCγ significantly attenuated neuropathic mechanical allodynia induced by spared nerve injury, whereas deletion of PKCα enhanced this allodynia. Baseline thermal and mechanical sensitivity, nociceptive behaviors induced by formalin, mechanical allodynia induced by complete Freund's adjuvant injection, were not altered by deletion of PKCα, β, γ, or δ. Finally, morphine analgesia and the development of morphine tolerance were not altered in PKCγ-deficient mice.
conclusionsPKC has isozyme-specific effects in pain modulation.
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Registered trials
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.