Astrocytic YAP prevents the glutamate neurotoxicity by upregulation of EAAT2 expression and promotes the gain of stemness in astrocytes in ischemic stroke mice.

ABSTRACT: The excessive glutamate-mediated excitotoxicity is a major cause of the neuron death in ischemic stroke (IS). Astrocytic glutamate transporter protein-1 (GLT-1, also named excitatory amino acid transporter 2, EAAT2) is essential for maintaining low extracellular glutamate and preventing glutamate neurotoxicity, while its expression is regulated by Yes-associated protein (YAP) signaling reported by our previous study. Recent studies have shown that ischemic injury of the brain induces the gain of stemness in astrocytes dependent on the de novo DNA methyltransferase DNMT3A, and YAP signaling contributes to DNA methylation remodeling upon mouse embryonic stem cell differentiation. However, it remains unknown the roles of astrocytic YAP signaling in IS and whether it regulates the glutamate-me

SUBMITTER: Luo X 

PROVIDER: S-EPMC12310981 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature