Functional human heme oxygenase has a neuroprotective effect on adult rat ganglion cells after pressure-induced ischemia.

Adult retina subjected to transient ischemia and reperfusion leads to controlled retinal ganglion cell (RGC) death over a period. Modification of intracellular mechanisms through a specific adenoviral vector containing the hemoxygenase gene (HO-1) provides avenues for RGC survival following HO-1 gene transfer and ischemia. RGC death rate was reduced by an average of 15% at 1, 2 and 3 weeks. A significant number of RGC transfected with functional HO-1 survived ischemic insults. Pharmacological stimulation of HO-1 may constitute a novel therapeutic approach to rescuing RGC experiencing ischemic/reperfusion injury.