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Increased oligodendrogenesis by humanin promotes axonal remyelination and neurological recovery in hypoxic/ischemic brains
Author(s) -
Chen Jing,
Sun Miao,
Zhang Xia,
Miao Zhigang,
Chua Balvin H. L.,
Hamdy Ronald C.,
Zhang QuanGuang,
Liu ChunFeng,
Xu Xingshun
Publication year - 2015
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.22350
Subject(s) - olig2 , remyelination , oligodendrocyte , corpus callosum , white matter , neurotrophic factors , neuroscience , atrophy , medicine , psychology , myelin , magnetic resonance imaging , central nervous system , receptor , radiology
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. © 2014 Wiley Periodicals, Inc.