ArticleMolecular pain2009
NF-kappaB mediated enhancement of potassium currents by the chemokine CXCL1/growth related oncogene in small diameter rat sensory neurons.
Article in Molecular pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- SOX11-mediated CBLN2 Upregulation Contributes to Neuropathic Pain through NF-κB-Driven Neuroinflammation in Dorsal Root Ganglia of Mice.Neuroscience bulletin · 2025Article
- Reparixin as a Potential Antiepileptogenic Agent: Modulation of the CXCL1-CXCR1/2 Axis and Seizure Activity in a Kindling Rat Model of Temporal Lobe Epilepsy.International journal of molecular sciences · 2025Article
- Establishment of a novel cellular model for Alzheimer's disease in vitro studies.Experimental neurology · 2024Article
- Afferent neurons of the kidney with impaired firing pattern in inflammation - role of sodium currents?Pflugers Archiv : European journal of physiology · 2023Article
- The Yin/Yang Balance of Communication between Sensory Neurons and Macrophages in Traumatic Peripheral Neuropathic Pain.International journal of molecular sciences · 2022Review
- The Importance of CXCL1 in Physiology and Noncancerous Diseases of Bone, Bone Marrow, Muscle and the Nervous System.International journal of molecular sciences · 2022Review
- CXCL10/CXCR3 Signaling in the DRG Exacerbates Neuropathic Pain in Mice.Neuroscience bulletin · 2021Article
- Pharmacological Blockade of Spinal CXCL3/CXCR2 Signaling by NVP CXCR2 20, a Selective CXCR2 Antagonist, Reduces Neuropathic Pain Following Peripheral Nerve Injury.Frontiers in immunology · 2019Article
- Correlation between the expression of IL‑18 and deep venous thrombosis.International journal of molecular medicine · 2018Article
- CXCL13/CXCR5 enhances sodium channel Nav1.8 current density via p38 MAP kinase in primary sensory neurons following inflammatory pain.Scientific reports · 2016Article
- Autoantibodies to citrullinated proteins induce joint pain independent of inflammation via a chemokine-dependent mechanism.Annals of the rheumatic diseases · 2016Article
- JNK in spinal cord facilitates bone cancer pain in rats through modulation of CXCL1.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016Article
- Mineralocorticoid Receptor, A Promising Target for Improving Management of Low Back Pain by Epidural Steroid Injections.Journal of anesthesia and perioperative medicine · 2016Article
- Overexpression of GRK6 attenuates neuropathic pain via suppression of CXCR2 in rat dorsal root ganglion.Molecular pain · 2016Article
- Chemokine CXCL1 enhances inflammatory pain and increases NMDA receptor activity and COX-2 expression in spinal cord neurons via activation of CXCR2.Experimental neurology · 2014Article
- Epigenetic modification of DRG neuronal gene expression subsequent to nerve injury: etiological contribution to complex regional pain syndromes (Part II).Medical science monitor : international medical journal of experimental and clinical research · 2014Review
- Painful, degenerating intervertebral discs up-regulate neurite sprouting and CGRP through nociceptive factors.Journal of cellular and molecular medicine · 2014Article
- NFκB-mediated CXCL1 production in spinal cord astrocytes contributes to the maintenance of bone cancer pain in mice.Journal of neuroinflammation · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInflammatory processes play important roles in both neuropathic and inflammatory pain states, but the effects of inflammation per se within the sensory ganglia are not well understood. The cytokine growth-related oncogene (GRO/KC; CXCL1) shows strong, rapid upregulation in dorsal root ganglion (DRG) in both nerve injury and inflammatory pain models. We examined the direct effects of GRO/KC on small diameter DRG neurons, which are predominantly nociceptive. Whole cell voltage clamp technique was used to measure voltage-activated potassium (K) currents in acutely cultured adult rat small diameter sensory neurons. Fluorescently labeled isolectin B4 (IB4) was used to classify cells as IB4-positive or IB4-negative.
resultsIn IB4-negative neurons, voltage-activated K current densities of both transient and sustained components were increased after overnight incubation with GRO/KC (1.5 nM), without marked changes in voltage dependence or kinetics. The average values for the slow and fast decay time constants at 20 mV were unchanged by GRO/KC. The amplitude of the fast inactivating component increased significantly with no large shifts in the voltage dependence of inactivation. The increase in K currents was completely blocked by co-incubation with protein synthesis inhibitor cycloheximide (CHX) or NF-kappaB inhibitors pyrrolidine dithiocarbamate (PDTC) or quinazoline (6-Amino-4-(4-phenoxypheny lethylamino;QNZ). In contrast, the voltage-activated K current of IB4-positive neurons was unchanged by GRO/KC. GRO/KC incubation caused no significant changes in the expression level of eight selected voltage-gated K channel genes in quantitative PCR analysis.
conclusionThe results suggest that GRO/KC has important effects in inflammatory processes via its direct actions on sensory neurons, and that activation of NF-kappaB is involved in the GRO/KC-induced enhancement of K currents.
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