Toxic Role of Heme Oxygenase in Hemorrhage

JHU scientists have investigated the contribution of inducible HO-1 to early brain injury produced by intracerebral hemorrhage (ICH). In vivo studies determined that after induction of ICH, HO-1 proteins are highly detectable in the peri-ICH region predominantly in microglia/macrophages and endothelial cells. Injury volume was found to be significantly smaller in HO-1 knockout (HO-1-/-) mice than in wildtype controls 24 and 72 h after ICH. The protection in HO-1-/-mice was associated with a marked reduction in ICH-induced leukocyte infiltration, microglia/macrophage activation, and free radical levels. These data reveal a previously unrecognized role of HO-1 in early brain injury after ICH. Thus, modulation of HO-1 signaling should be assessed further in clinical settings, especially for hemorrhagic states. Description (Set) Proposed Use (Set) Identifying ways to decrease heme oxygenase 1 activity would limit damage following hemorrhage, especially in intra-cerebral hemorrhage. The use of a heme oxygenase inhibitor, or a means to decrease heme oxygenase-1 levels would decrease generation of high toxic levels of heme metabolites

Inventor(s): Dore, Sylvain

Type of Offer: Licensing



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