PMID- 30120407
OWN - NLM
STAT- MEDLINE
DCOM- 20200312
LR  - 20200312
IS  - 1530-0447 (Electronic)
IS  - 0031-3998 (Linking)
VI  - 85
IP  - 1
DP  - 2019 Jan
TI  - The neurorestorative effect of human amniotic fluid stem cells on the chronic 
      phase of neonatal hypoxic-ischemic encephalopathy in mice.
PG  - 97-104
LID - 10.1038/s41390-018-0131-8 [doi]
AB  - BACKGROUND: Hypoxic-ischemic encephalopathy (HIE) remains a major cause of 
      cerebral palsy. Increasing evidence has suggested that mesenchymal stem cells 
      have a favorable effect on HIE. However, the efficacy of human amniotic fluid 
      stem cells (hAFS) for HIE, especially in the chronic phase, remains unclear. The 
      aim of this study was to determine the neurorestorative effect of hAFS on the 
      chronic phase of HIE. METHODS: hAFS were isolated from AF cells as CD117-positive 
      cells. HI was induced in 9-day-old mice. Animals intranasally received hAFS or 
      phosphate-buffered saline at 10 days post HI and were harvested for histological 
      analysis after functional tests at 21 days post HI. We also implanted 
      PKH26-positive hAFS to assess their migration to the brain. Finally, we 
      determined gene expressions of trophic factors in hAFS co-cultured with HI brain 
      extract. RESULTS: hAFS improved sensorimotor deficits in HIE by gray and white 
      matter restoration and neuroinflammation reduction followed by migration to the 
      lesion. Brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), 
      hepatocyte growth factor (HGF), and stromal cell-derived factor-1 (SDF-1) gene 
      expressions in hAFS were elevated when exposed to HI-induced brain extract. 
      CONCLUSION: hAFS induced functional recovery by exerting neurorestorative effects 
      in HIE mice, suggesting that intranasal administration of hAFS could be a novel 
      treatment for HIE, especially in the chronic phase.
FAU - Otani, Toshimitsu
AU  - Otani T
AD  - Department of Obstetrics and Gynecology, Keio University School of Medicine, 
      Tokyo, Japan.
FAU - Ochiai, Daigo
AU  - Ochiai D
AD  - Department of Obstetrics and Gynecology, Keio University School of Medicine, 
      Tokyo, Japan. ochiaidaigo@keio.jp.
FAU - Masuda, Hirotaka
AU  - Masuda H
AD  - Department of Obstetrics and Gynecology, Keio University School of Medicine, 
      Tokyo, Japan.
FAU - Abe, Yushi
AU  - Abe Y
AD  - Department of Obstetrics and Gynecology, Keio University School of Medicine, 
      Tokyo, Japan.
FAU - Fukutake, Marie
AU  - Fukutake M
AD  - Department of Obstetrics and Gynecology, Keio University School of Medicine, 
      Tokyo, Japan.
FAU - Matsumoto, Tadashi
AU  - Matsumoto T
AD  - Department of Obstetrics and Gynecology, Keio University School of Medicine, 
      Tokyo, Japan.
FAU - Miyakoshi, Kei
AU  - Miyakoshi K
AD  - Department of Obstetrics and Gynecology, Keio University School of Medicine, 
      Tokyo, Japan.
FAU - Tanaka, Mamoru
AU  - Tanaka M
AD  - Department of Obstetrics and Gynecology, Keio University School of Medicine, 
      Tokyo, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180810
PL  - United States
TA  - Pediatr Res
JT  - Pediatric research
JID - 0100714
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (CXCL12 protein, human)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (HGF protein, human)
RN  - 0 (NGF protein, human)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.10.1 (KIT protein, human)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
SB  - IM
MH  - Amniotic Fluid/*cytology
MH  - Animals
MH  - Animals, Newborn
MH  - Behavior, Animal
MH  - Brain/metabolism/pathology/*physiopathology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cell Movement
MH  - Cells, Cultured
MH  - Chemokine CXCL12/metabolism
MH  - Disease Models, Animal
MH  - Hepatocyte Growth Factor/metabolism
MH  - Humans
MH  - Hypoxia-Ischemia, Brain/metabolism/pathology/physiopathology/*surgery
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Motor Activity
MH  - Nerve Growth Factor/metabolism
MH  - Neural Stem Cells/metabolism/*transplantation
MH  - *Neurogenesis
MH  - Proto-Oncogene Proteins c-kit/metabolism
MH  - Signal Transduction
EDAT- 2018/08/19 06:00
MHDA- 2020/03/13 06:00
CRDT- 2018/08/19 06:00
PHST- 2018/03/16 00:00 [received]
PHST- 2018/07/22 00:00 [accepted]
PHST- 2018/06/25 00:00 [revised]
PHST- 2018/08/19 06:00 [pubmed]
PHST- 2020/03/13 06:00 [medline]
PHST- 2018/08/19 06:00 [entrez]
AID - 10.1038/s41390-018-0131-8 [pii]
AID - 10.1038/s41390-018-0131-8 [doi]
PST - ppublish
SO  - Pediatr Res. 2019 Jan;85(1):97-104. doi: 10.1038/s41390-018-0131-8. Epub 2018 Aug 
      10.