Combined effect of hypothermia and caspase-2 gene deficiency on neonatal hypoxic–ischemic brain injury View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-02-09

AUTHORS

Ylva Carlsson, Xiaoyang Wang, Leslie Schwendimann, Catherine I. Rousset, Etienne Jacotot, Pierre Gressens, Marianne Thoresen, Carina Mallard, Henrik Hagberg

ABSTRACT

Intoduction:Hypoxia–ischemia (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 (NE), saving one in nine infants from developing neurological deficits. Caspase-2 is an initiator caspase, a key enzyme in the route to destruction and, therefore, theoretically a potential target for a pharmaceutical strategy to prevent HI brain damage.Methods:The aim of this study was to explore the neuroprotective efficacy of hypothermia in combination with caspase-2 gene deficiency using the neonatal Rice–Vannucci model of HI injury in mice.Results:HI brain injury was moderately reduced in caspase-2−/− mice as compared with wild-type (WT) mice. Five hours of hypothermia (33 °C ) vs. normothermia (36 °C) directly after HI provided additive protection overall (temperature P = 0.0004, caspase-2 genotype P = 0.0029), in the hippocampus and thalamus, but not in other gray matter regions or white matter. Delayed hypothermia initiated 2 h after HI in combination with caspase-2 gene deficiency reduced injury in the hippocampus, but not in other brain areas.Discussion:In conclusion, caspase-2 gene deficiency combined with hypothermia provided enhanced neuroprotection as compared with hypothermia alone. More... »

PAGES

566-572

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/pr.2012.15

DOI

http://dx.doi.org/10.1038/pr.2012.15

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008706942

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22322383


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