Combined effect of hypothermia and Caspase-2 gene deficiency on neonatal hypoxic-ischemic brain injury

Y Carlsson, X Wang, L Schwendimann, CI Rousset, E Jacotot, P Gressens, M Thoresen, C Mallard, H Hagberg

Research output: Contribution to journalArticle (Academic Journal)peer-review

21 Citations (Scopus)

Abstract

Hypoxic-ischemic (HI) injury in term infants develops with a delay during the recovery phase, opening up a therapeutic window after the insult. Hypothermia is currently an established neuroprotective treatment in newborns with neonatal encephalopathy saving 1 infant in 9 from developing neurological deficits. The aim of the present study was to explore the neuroprotective efficacy of hypothermia in combination with caspase-2 gene deficiency in a mouse model of HI. HI brain injury was significantly lower in caspase-2-/- animals compared with heterozygotes and wild-type animals. Administration of 5 h of hypothermia directly after HI provided additional protection in mice with caspase-2 gene deletion (temperature p=0.0004, genotype p=0.0029). This was especially noticeable in hippocampus and thalamus. Hypothermia protected wild-type animals to the same degree as that provided by caspase-2 gene deletion alone. Even hypothermia delayed 2 h after HI offered protection in this neonatal mouse model of HI, decreasing both gray (p=0.0486) and white matter (p=0.02) injury. In conclusion, caspase-2 gene deficiency combined with hypothermia provided stronger neuroprotection than hypothermia alone.
Translated title of the contributionCombined effect of hypothermia and Caspase-2 gene deficiency on neonatal hypoxic-ischemic brain injury
Original languageEnglish
Article numbere-pub Feb 2012
Pages (from-to)566-572
Number of pages7
JournalPediatric Research
Volume71
Issue number5
Early online date9 Feb 2012
DOIs
Publication statusPublished - May 2012

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