title: Neuroprotective effect of heme oxygenase-2 knockout in the blood injection model of intracerebral hemorrhage.
abstract: BACKGROUND
  The toxicity of heme breakdown products may contribute to the pathogenesis of intracerebral hemorrhage (ICH). Heme catabolism is catalyzed by the heme oxygenase enzymes. We have previously reported that heme oxygenase-2 (HO-2), the constitutive isoform, protects neurons from hemin in vitro and reduces oxidative stress after striatal blood injection. In order to further evaluate HO-2 as a therapeutic target, we tested the hypothesis that HO-2 gene deletion protects neurons and attenuates behavioral deficits after ICH.
  
  
  RESULTS
  Injection of 20 μl blood into the right striatum of HO-2 wild-type mice resulted in loss of approximately one third of striatal neurons 4-8 days later. Neuronal survival was significantly increased in HO-2 knockout mice at both time points. This was associated with reduced motor deficit as detected by the corner test; however, no differences were detected in spontaneous activity or the adhesive removal or elevated body swing tests.
  
  
  CONCLUSIONS
  HO-2 knockout attenuates perihematomal neuron loss in the blood injection ICH model, but has a weak and variable effect on neurological outcome.
authors.forename: Jing
authors.initials: J
authors.lastname: Chen-Roetling
authors.forename: Ying
authors.initials: Y
authors.lastname: Cai
authors.affiliation: Department of Emergency Medicine, Thomas Jefferson University, 1025 Walnut Street, College Building Room 813, Philadelphia, PA 19107, USA. Raymond.Regan@jefferson.edu.
authors.forename: Raymond F
authors.initials: RF
authors.lastname: Regan
mesh_terms: D000818:Animals; D002543:Cerebral Hemorrhage / Q000201:enzymology* / Q000235:genetics; D006419:Heme Oxygenase (Decyclizing) / Q000235:genetics*; D051379:Mice; D018345:Mice, Knockout
chemical_list: D006419:Heme Oxygenase (Decyclizing); C105245:heme oxygenase-2