RHBDF2 governs microglial neuroinflammation during cerebral ischemia-reperfusion injury and is positively regulated by the m6A reader YTHDF1.

ABSTRACT:

Background

Neuroinflammation mediated by microglia activation is the key pathological mechanisms for cerebral ischemia-reperfusion injury (CIRI). This study investigated the role and underlying molecular mechanism of Rhomboid 5 homolog 2 (RHBDF2) in neuroinflammation during CIRI.

Methods

The in vivo middle cerebral artery occlusion and reperfusion (MCAO/R) mouse model and in vitro HMC3 microglia subjected to oxygen glucose deprivation and reperfusion (OGD/R) were established to mimic CIRI. Real-time PCR, western blot, immunohistochemistry, immunofluorescence, flow cytometry, and co-immunoprecipitation assays were used to confirm RHBDF2 expression and explore the molecular mechanism of microglia-specific RHBDF2 knockdown in CIRI. Methylated RNA immunoprecipitation was used to

SUBMITTER: Xu L 

PROVIDER: S-EPMC12403488 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature