Integrative transcriptomic analysis reveals Cd72 as a novel pro-inflammatory factor in microglia following experimental ischemic stroke

Ischemic stroke remains a leading cause of global mortality and disability, with neuroinflammation playing a critical role in determining patient outcomes. Microglia, the brain's resident immune cells, can both exacerbate neuroinflammation and neuronal damage by releasing neurotoxic mediators and engaging in excessive phagocytosis, while also aiding recovery through the production of anti-inflammatory cytokines and debris clearance. However, the molecular mechanisms governing microglial activation and polarization after ischemic stroke are not well elucidated. In this study, we combined integrative transcriptomic analyses with experimental validation in a murine model of middle cerebral artery occlusion/reperfusion (MCAO/R) to explore microglial heterogeneity and identify key regulatory factors in ischemic stroke. Bioinformatics analysis identified Cd72 as a novel pro-inflammatory modulator within ischemia-associated microglial phenotypes. We observed significant upregulation of Cd72 in microglia following MCAO/R, and selective knockdown of Cd72 using CX3CR1