Blocking CK2α‐Bclaf1 Preserves Oligodendrocytes After Neonatal Hypoxic Injury

ABSTRACT: Neonatal hypoxic injury is a common disorder that disrupts white matter development in newborns, with long-term impacts on cognitive and mental function. While oxygen availability controls oligodendrocyte (OL) differentiation, prolonged hypoxia leads to OL death and impairs subsequent myelination even after returning to normoxic conditions. In this study, we uncovered dual roles of the serine/threonine kinase CK2α and the transcriptional factor Bclaf1 in OL differentiation in an oxygen-dependent manner. Phosphorylated Bclaf1 by CK2α is essential for normal OL function. On the contrary, the CK2α-Bclaf1 axis drives hypoxia-induced OL apoptosis and alters the post-hypoxic myelination process. Importantly, inhibiting Bclaf1 activity with the acute treatment of clinically approved CK2 inhibitor silmitasertib and the herbal supplement curcumin protects OLs and restores myelin production in newborns following hypoxic injury. This approach unveils a key transcriptional mechanism in OL development and highlights a potential therapeutic strategy to mitigate neonatal hypoxic injury and prevent long-term mental health complications.

ORGANISM(S): Mus musculus

PROVIDER: GSE288101 | GEO | 2026/07/31

REPOSITORIES: GEO