ArticleMolecular pain
Pharmacological inhibition of MKP-1 exacerbates central post-stroke pain and neuroinflammation in mice.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Central post-stroke pain (CPSP) remains difficult to treat due to limited understanding of its underlying mechanisms. Emerging evidence implicates microglia-driven neuroinflammation in CPSP development. Mitogen-activated protein kinase phosphatase-1 (MKP-1) negatively regulates MAPK signaling and modulates inflammation in neurological disorders, yet its role in CPSP is unclear. Using a mouse model of thalamic hemorrhage, we examined MKP-1 expression and function in CPSP. Behavioral testing assessed pain hypersensitivity and affective disturbances. Immunofluorescence and western blot evaluated MKP-1 expression, microglial activation, and inflammatory signaling in the thalamus. Pharmacological MKP-1 inhibition was employed to assess functional contributions. Thalamic hemorrhage induced persistent mechanical hypersensitivity and anxiety-like behaviors, accompanied by pronounced microglial activation in the peri-lesional thalamus. MKP-1 expression increased significantly after stroke and localized primarily to microglia. MKP-1 inhibition exacerbated pain behaviors and enhanced microglial activation, with corresponding increases in pro-inflammatory mediators and p38 MAPK phosphorylation. These findings suggest that MKP-1 may function as an endogenous negative regulator of microglia-mediated neuroinflammation following thalamic hemorrhage. Pharmacological modulation of MKP-1 signaling warrants further investigation as a potential approach for CPSP.
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