Increased oligodendrogenesis by humanin promotes axonal remyelination and neurological recovery in hypoxic/ischemic brains

Jing Chen, Miao Sun, Xia Zhang, Zhigang Miao, Balvin H.L. Chua, Ronald C. Hamdy, Quanguang Zhang, Chun Feng Liu, Xingshun Xu

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

Oligodendrocytes are the predominant cell type in white matter and are highly vulnerable to ischemic injury. The role of oligodendrocyte dysfunction in ischemic brain injury is unknown. In this study, we used a 24-amino acid peptide S14G-Humanin (HNG) to examine oligodendrogenesis and neurological functional recovery in a hypoxic/ischemic (H/I) neonatal model. Intraperitoneal HNG pre-treatment decreased infarct volume following H/I injury. Delayed HNG treatment 24 h after H/I injury did not reduce infarct volume but did decrease neurological deficits and brain atrophy. Delayed HNG treatment did not attenuate axonal demyelination at 48 h after H/I injury. However, at 14 d after H/I injury, delayed HNG treatment increased axonal remyelination, the thickness of corpus callosum at the midline, the number of Olig2+/BrdU+ cells, and levels of brain-derived neurotrophic factor (BDNF). Our results suggest that targeting oligodendrogenesis via delayed HNG treatment may represent a promising approach for the treatment of stroke.

Original languageEnglish (US)
Pages (from-to)62-71
Number of pages10
JournalHippocampus
Volume25
Issue number1
DOIs
StatePublished - Jan 1 2015

Keywords

  • Brain-derived neurotrophic factor
  • Humanin
  • Hypoxic/ischemic injury
  • Oligodendrocyte
  • Remyelination

ASJC Scopus subject areas

  • Cognitive Neuroscience

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