Document Type


Publication Date



This article has been peer reviewed. It was published in: BMC Research Notes.

Volume 7, Issue 1, 22 August 2014, Article number 561.

The published version is available at DOI: 10.1186/1756-0500-7-561.

Copyright © Chen-Roetling et al.; licensee BioMed Central Ltd. 2014


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.

FINDINGS: 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.

CONCLUSION: HO-2 knockout attenuates perihematomal neuron loss in the blood injection ICH model, but has a weak and variable effect on neurological outcome.

PubMed ID