PMID- 28561815
OWN - NLM
STAT- MEDLINE
DCOM- 20180516
LR  - 20190610
IS  - 1530-0447 (Electronic)
IS  - 0031-3998 (Print)
IS  - 0031-3998 (Linking)
VI  - 82
IP  - 3
DP  - 2017 Sep
TI  - Effects of therapeutic hypothermia on white matter injury from murine neonatal 
      hypoxia-ischemia.
PG  - 518-526
LID - 10.1038/pr.2017.75 [doi]
AB  - BackgroundTherapeutic hypothermia (TH) is the standard of care for neonates with 
      hypoxic-ischemic encephalopathy, but it is not fully protective in the clinical 
      setting. Hypoxia-ischemia (HI) may cause white matter injury (WMI), leading to 
      neurological and cognitive dysfunction.MethodsP9 mice were subjected to HI as 
      previously described. Pups underwent 3.5 h of systemic hypothermia or 
      normothermia. Cresyl violet and Perl's iron staining for histopathological 
      scoring of brain sections was completed blindly on all brains. Immunocytochemical 
      (ICC) staining for myelin basic protein (MBP), microglia (Iba1), and astrocytes 
      (glia fibrillary acidic protein (GFAP)) was performed on adjacent sections. 
      Volumetric measurements of MBP coverage were used for quantitative analysis of 
      white matter.ResultsTH provided neuroprotection by injury scoring for the entire 
      group (n=44; P<0.0002). ICC analysis of a subset of brains showed that the 
      lateral caudate was protected from WMI (P<0.05). Analysis revealed decreased GFAP 
      and Iba1 staining in hippocampal regions, mostly CA2/CA3. GFAP and Iba1 directly 
      correlated with injury scores of normothermic brains.ConclusionTH reduced injury, 
      and qualitative data suggest that hippocampus and lateral caudate are protected 
      from HI. Mildly injured brains may better show the benefits of TH. Overall, these 
      data indicate regional differences in WMI susceptibility and inflammation in a P9 
      murine HI model.
FAU - Koo, Elliot
AU  - Koo E
AD  - Department of Pediatrics, University of California San Francisco, San Francisco, 
      California.
FAU - Sheldon, R Ann
AU  - Sheldon RA
AD  - Department of Pediatrics, University of California San Francisco, San Francisco, 
      California.
FAU - Lee, Byong Sop
AU  - Lee BS
AD  - Department of Neurology, University of Ulsan College of Medicine, Seoul, Korea.
FAU - Vexler, Zinaida S
AU  - Vexler ZS
AD  - Department of Neurology, University of California San Francisco, San Francisco, 
      California.
FAU - Ferriero, Donna M
AU  - Ferriero DM
AD  - Department of Pediatrics, University of California San Francisco, San Francisco, 
      California.
LA  - eng
GR  - P50 NS035902/NS/NINDS NIH HHS/United States
GR  - R01 NS033997/NS/NINDS NIH HHS/United States
GR  - R01 NS044025/NS/NINDS NIH HHS/United States
GR  - R01 NS076726/NS/NINDS NIH HHS/United States
PT  - Journal Article
DEP - 20170531
PL  - United States
TA  - Pediatr Res
JT  - Pediatric research
JID - 0100714
RN  - 0 (Glial Fibrillary Acidic Protein)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Female
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - *Hypothermia, Induced
MH  - Hypoxia-Ischemia, Brain/metabolism/pathology/*therapy
MH  - Male
MH  - Mice
MH  - White Matter/metabolism/*pathology
PMC - PMC5570671
MID - NIHMS859417
EDAT- 2017/06/01 06:00
MHDA- 2018/05/17 06:00
PMCR- 2017/11/30
CRDT- 2017/06/01 06:00
PHST- 2016/10/10 00:00 [received]
PHST- 2017/03/06 00:00 [accepted]
PHST- 2017/06/01 06:00 [pubmed]
PHST- 2018/05/17 06:00 [medline]
PHST- 2017/06/01 06:00 [entrez]
PHST- 2017/11/30 00:00 [pmc-release]
AID - pr201775 [pii]
AID - 10.1038/pr.2017.75 [doi]
PST - ppublish
SO  - Pediatr Res. 2017 Sep;82(3):518-526. doi: 10.1038/pr.2017.75. Epub 2017 May 31.