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Related Experiment Video

Updated: Jul 3, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

Blocking CK2α-Bclaf1 Preserves Oligodendrocytes After Neonatal Hypoxic Injury.

Chien-Fang Huang1, Ti-Jie Yuan1, Ming-Yi Lin1

  • 1Department of Biotechnology and Bioindustry Sciences, National Cheng Kung University, Tainan, Taiwan.

Glia
|July 2, 2026
PubMed
Summary

Neonatal hypoxic injury kills oligodendrocytes (OLs) by activating CK2α-Bclaf1. Therapies targeting this pathway may protect developing brains and prevent cognitive deficits.

Keywords:
curcuminhypoxiaoligodendrocytesilmitasertibwhite matter injury

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Progenitor-derived Oligodendrocyte Culture System from Human Fetal Brain
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Last Updated: Jul 3, 2026

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07:36

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Published on: November 20, 2015

Preparation of Rat Oligodendrocyte Progenitor Cultures and Quantification of Oligodendrogenesis Using Dual-infrared Fluorescence Scanning
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Progenitor-derived Oligodendrocyte Culture System from Human Fetal Brain
14:26

Progenitor-derived Oligodendrocyte Culture System from Human Fetal Brain

Published on: December 20, 2012

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cellular Pathology

Background:

  • Neonatal hypoxic injury impairs white matter development in preterm infants, causing long-term cognitive and mental deficits.
  • Prolonged hypoxia leads to oligodendrocyte (OL) death and delayed myelination, even after oxygen levels normalize.

Purpose of the Study:

  • To investigate the roles of serine/threonine kinase CK2α and transcription factor Bclaf1 in OL survival during hypoxia.
  • To identify potential therapeutic targets for mitigating hypoxia-induced OL damage in newborns.

Main Methods:

  • Examined the interaction between CK2α and Bclaf1 under hypoxic conditions.
  • Assessed the impact of Vhl (hypoxia-inducible E3 ligase) on OL apoptosis.
  • Evaluated the protective effects of CK2 inhibitor silmitasertib and curcumin on OLs in a neonatal hypoxic injury model.

Main Results:

  • CK2α-mediated phosphorylation of Bclaf1 promotes hypoxia-induced OL apoptosis.
  • Restoring Vhl expression reversed hypoxia-mediated OL death.
  • Silmitasertib and curcumin treatment protected OLs and preserved pre-myelinating capacity after hypoxic injury.

Conclusions:

  • CK2α and Bclaf1 are key regulators of OL apoptosis in neonatal hypoxic injury.
  • Targeting the CK2α-Bclaf1 pathway offers a potential therapeutic strategy for neonatal hypoxic brain injury.
  • Silmitasertib and curcumin show promise in protecting developing white matter from hypoxic damage.