Project DetailsCells, tissues, organs, and species respond to stress by adaptations that render them more resistant to that same stress. Scientists are now capitalizing on this fundamental response, learning how cells defend themselves when presented with a mild stress, so as to better design therapeutics for true disease. Recently, it was learned that stressing the retina by having mice breath air with a low oxygen content (hypoxia) significantly reduces the death of ganglion cells in the retina when the mice develop experimental glaucoma. These findings imply that genes endogenous to these cells might be activated for glaucoma protection. The present study will focus on heme oxygenase-1, a protein believed to be responsible for the protection of hypoxia-stressed retinal ganglion cells in glaucoma. Dr. Gidday will make extensive determinations of how retinal hypoxia changes the expression of this protein, and will study mice missing or overexpressing this gene to confirm its participation in the protection. Heme oxygenase-1 therapy might represent a new treatment strategy for patients with glaucoma.