ArticleMolecular pain2012
Mitogen activated protein kinase phosphatase-1 prevents the development of tactile sensitivity in a rodent model of neuropathic pain.
Article in Molecular pain, 2012. 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, 33 citations in OpenAlex.
- Downregulation of dual-specificity phosphatase 1 (DUSP1) in post-mortem brain white matter in progressive multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- mPFC DUSP1 mediates adolescent cocaine exposure-induced higher sensitivity to drug in adulthood.EMBO reports · 2023Article
- Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2Nature neuroscience · 2022Article
- MiR-101 promotes pain hypersensitivity in rats with chronic constriction injury via the MKP-1 mediated MAPK pathway.Journal of cellular and molecular medicine · 2020Article
- Dual-Specificity Phosphatase Regulation in Neurons and Glial Cells.International journal of molecular sciences · 2019Review
- Macrophage-specific nanotechnology-driven CD163 overexpression in human macrophages results in an M2 phenotype under inflammatory conditions.Immunobiology · 2017Article
- Neuropathic pain promotes adaptive changes in gene expression in brain networks involved in stress and depression.Science signaling · 2017Article
- Evaluation of a nanotechnology-based approach to induce gene-expression in human THP-1 macrophages under inflammatory conditions.Immunobiology · 2017Article
- Current and Future Issues in the Development of Spinal Agents for the Management of Pain.Current neuropharmacology · 2017Review
- Mitogen-activated protein kinase phosphatase-3 (MKP-3) in the surgical wound is necessary for the resolution of postoperative pain in mice.Journal of pain research · 2017Article
- A role for mitogen-activated protein kinase phosphatase 1 (MKP1) in neural cell development and survival.Neural regeneration research · 2015Article
- The search for novel analgesics: targets and mechanisms.F1000prime reports · 2015Review
- Mitogen-Activated Protein Kinase Phosphatase (MKP)-1 in Nervous System Development and Disease.Molecular neurobiology · 2015Review
- Genomewide analysis of rat periaqueductal gray-dorsal horn reveals time-, region- and frequency-specific mRNA expression changes in response to electroacupuncture stimulation.Scientific reports · 2014Article
- Lost but making progress--Where will new analgesic drugs come from?Science translational medicine · 2014Review
- 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
- Mitogen-activated protein kinase (MAPK) phosphatase-3 (MKP-3) displays a p-JNK-MAPK substrate preference in astrocytes in vitro.Neuroscience letters · 2014Article
- A novel p38 MAPK docking-groove-targeted compound is a potent inhibitor of inflammatory hyperalgesia.The Biochemical journal · 2014Article
- Pathological pain and the neuroimmune interface.Nature reviews. Immunology · 2014Review
- Glia and pain: is chronic pain a gliopathy?Pain · 2013Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNeuropathic pain due to nerve injury is one of the most difficult types of pain to treat. Following peripheral nerve injury, neuronal and glial plastic changes contribute to central sensitization and perpetuation of mechanical hypersensitivity in rodents. The mitogen activated protein kinase (MAPK) family is pivotal in this spinal cord plasticity. MAPK phosphatases (MKPs) limit inflammatory processes by dephosphorylating MAPKs. For example, MKP-1 preferentially dephosphorylates p-p38. Since spinal p-p38 is pivotal for the development of chronic hypersensitivity in rodent models of pain, and p-p38 inhibitors have shown clinical potential in acute and chronic pain patients, we hypothesize that induction of spinal MKP-1 will prevent the development of peripheral nerve-injury-induced hypersensitivity and p-p38 overexpression.
resultsWe cloned rat spinal cord MKP-1 and optimize MKP-1 cDNA in vitro using transfections to BV-2 cells. We observed that in vitro overexpression of MKP-1 blocked lipopolysaccharide-induced phosphorylation of p38 (and other MAPKs) as well as release of pro-algesic effectors (i.e., cytokines, chemokines, nitric oxide). Using this cDNA MKP-1 and a non-viral, in vivo nanoparticle transfection approach, we found that spinal cord overexpression of MKP-1 prevented development of peripheral nerve-injury-induced tactile hypersensitivity and reduced pro-inflammatory cytokines and chemokines and the phosphorylated form of p38.
conclusionsOur results indicate that MKP-1, the natural regulator of p-p38, mediates resolution of the spinal cord pro-inflammatory milieu induced by peripheral nerve injury, resulting in prevention of chronic mechanical hypersensitivity. We propose that MKP-1 is a potential therapeutic target for pain treatment or prevention.
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