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

5 Citations (Scopus)

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

Fingerprint

Wounds and Injuries
Brain
Oligodendroglia
Corpus Callosum
Brain-Derived Neurotrophic Factor
Demyelinating Diseases
Bromodeoxyuridine
Brain Injuries
Atrophy
Stroke
humanin
Amino Acids
Peptides
Mice Gly(14)-Humanin
White Matter

Keywords

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

ASJC Scopus subject areas

  • Cognitive Neuroscience

Cite this

Increased oligodendrogenesis by humanin promotes axonal remyelination and neurological recovery in hypoxic/ischemic brains. / Chen, Jing; Sun, Miao; Zhang, Xia; Miao, Zhigang; Chua, Balvin H.L.; Hamdy, Ronald C.; Zhang, Quanguang; Liu, Chun Feng; Xu, Xingshun.

In: Hippocampus, Vol. 25, No. 1, 01.01.2015, p. 62-71.

Research output: Contribution to journalArticle

Chen, Jing ; Sun, Miao ; Zhang, Xia ; Miao, Zhigang ; Chua, Balvin H.L. ; Hamdy, Ronald C. ; Zhang, Quanguang ; Liu, Chun Feng ; Xu, Xingshun. / Increased oligodendrogenesis by humanin promotes axonal remyelination and neurological recovery in hypoxic/ischemic brains. In: Hippocampus. 2015 ; Vol. 25, No. 1. pp. 62-71.
@article{10207351be2b4aab99e81fe8f3180ae6,
title = "Increased oligodendrogenesis by humanin promotes axonal remyelination and neurological recovery in hypoxic/ischemic brains",
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.",
keywords = "Brain-derived neurotrophic factor, Humanin, Hypoxic/ischemic injury, Oligodendrocyte, Remyelination",
author = "Jing Chen and Miao Sun and Xia Zhang and Zhigang Miao and Chua, {Balvin H.L.} and Hamdy, {Ronald C.} and Quanguang Zhang and Liu, {Chun Feng} and Xingshun Xu",
year = "2015",
month = "1",
day = "1",
doi = "10.1002/hipo.22350",
language = "English (US)",
volume = "25",
pages = "62--71",
journal = "Hippocampus",
issn = "1050-9631",
publisher = "Wiley-Liss Inc.",
number = "1",

}

TY - JOUR

T1 - Increased oligodendrogenesis by humanin promotes axonal remyelination and neurological recovery in hypoxic/ischemic brains

AU - Chen, Jing

AU - Sun, Miao

AU - Zhang, Xia

AU - Miao, Zhigang

AU - Chua, Balvin H.L.

AU - Hamdy, Ronald C.

AU - Zhang, Quanguang

AU - Liu, Chun Feng

AU - Xu, Xingshun

PY - 2015/1/1

Y1 - 2015/1/1

N2 - 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.

AB - 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.

KW - Brain-derived neurotrophic factor

KW - Humanin

KW - Hypoxic/ischemic injury

KW - Oligodendrocyte

KW - Remyelination

UR - http://www.scopus.com/inward/record.url?scp=84917676701&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84917676701&partnerID=8YFLogxK

U2 - 10.1002/hipo.22350

DO - 10.1002/hipo.22350

M3 - Article

C2 - 25139533

AN - SCOPUS:84917676701

VL - 25

SP - 62

EP - 71

JO - Hippocampus

JF - Hippocampus

SN - 1050-9631

IS - 1

ER -