By Michael J. Parnham (auth.)
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Additional resources for Advantages and Problems with Non-Opioids in Pain Management: Vancouver, Canada, August 19, 1996
Hypothesis 3. Induction of HO-1 in spinal cord blood vessels, prior to injury, stabilizes the blood-spinal cord barrier, attenuates the early induction of vascular adhesion molecules and infiltration of inflammatory cells, and promotes functional recovery. Experiments: We will determine if systemic administration of heme prior to injury, a strategy which preferentially induces HO-1 in endothelium, will restrict barrier disruption to proteins, limit the infiltration of neutrophils through the modulation of vascular adhesion molecules, and promote locomotor recovery.
Iron deficiency is the most common human nutritional deficiency disease. At the same time excessive iron stores have been associated with increased occurrence of neurological disorders and certain cancers. Mammalian iron metabolism is modulated through the action of two regulatory RNA binding proteins, iron regulatory protein 1 (IRP1) and IRP2. IRPs bind to iron responsive elements (IRE) in ferritin (iron storage) and transferrin receptor (TfR) (iron uptake) mRNAs and regulate their translation or stability, respectively.
Preliminary experiments suggest that this discrepancy may be explained in part by the effects of two inducible antioxidants: heme oxygenase (HO)- and ferritin. The former is rapidly induced by Hb and may facilitate synthesis of L-rich ferritin in astrocytes. In contrast, Hb decreases the expression of L-rich ferritin in neurons; iron released as a product of heme breakdown may then be toxic. This project will address the role of HO and ferritin in cell culture and in vivo models. Overexpression of HO-1 will be accomplished in Studies 23 glial, neuronal, or mixed cultures via gene transfer; the relationship between activity, heme-mediated reactive oxygen species formation, and cell death will be established.