ArticleScientific reports2026
CD204 regulates microglial/macrophage M1/M2 polarization and alleviates neuroinflammation following intracerebral hemorrhage.
Article in Scientific reports, 2026. 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
Intracerebral hemorrhage (ICH) is a main cause of death and disability worldwide. Microglial/macrophage activation and neuroinflammation are key events following ICH, but the molecular mechanisms of mediator regulatory function are not well understood. Cluster of differentiation 204 (CD204), a macrophage scavenger receptor, regulates multiple features of microglial/macrophage physiology. However, its function in regulating the innate immune response and microglial/macrophage M1/M2 polarization in ICH has not been addressed. In the current study, we aimed to investigate whether CD204 is involved in the regulation of M1/M2 microglial/macrophage polarization and neuroinflammation following ICH. The ICH mouse model was employed. CD204 siRNA was intracerebroventricularly administered, and tamibarotene was intraperitoneally administered for intervention. The neurobehavioral assessments, RT-PCR, Western blot, immunohistochemistry, Nissl staining, and ELISA were performed. CD204 is upregulated and regulates microglial/macrophage M1/M2 polarization and neuroinflammation in ICH. Mechanistically, inhibition of CD204 markedly decreases microglial/macrophage M2-like polarization while increases M1-like polarization, which exacerbates the brain injury after ICH. Tamibarotene exerts beneficial effects in ICH mice through CD204 activation. CD204 plays an important role in M1/M2-macrophage/microglial polarization, providing novel potential therapeutic targets for the regulation of immune and inflammatory disorders in ICH.
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