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Abstract #80722 Published in IGR 20-3
Cell Autonomous Neuroprotection by the Mitochondrial Uncoupling Protein 2 in a Mouse Model of Glaucoma
Hass DT; Hass DT; Barnstable CJFrontiers in neuroscience 2019; 13: 201
Glaucoma is a group of disorders associated with retinal ganglion cell (RGC) degeneration and death. There is a clear contribution of mitochondrial dysfunction and oxidative stress toward glaucomatous RGC death. Mitochondrial uncoupling protein 2 () is a well-known regulator of oxidative stress that increases cell survival in acute models of oxidative damage. The impact of on cell survival during sub-acute and chronic neurodegenerative conditions, however, is not yet clear. Herein, we test the hypothesis that increased expression will improve RGC survival in a mouse model of glaucoma. We show that increasing RGC but not glial expression in transgenic animals decreases glaucomatous RGC death, but also that the PPAR-γ agonist rosiglitazone (RSG), an endogenous transcriptional activator of , does not significantly alter RGC loss during glaucoma. Together, these data support a model whereby increased expression mediates neuroprotection during a long-term oxidative stressor, but that transcriptional activation alone is insufficient to elicit a neuroprotective effect, motivating further research in to the post-transcriptional regulation of .
Department of Neural and Behavioral Sciences, College of Medicine, The Pennsylvania State University, Hershey, PA, United States.
Full articleClassification:
11.8 Neuroprotection (Part of: 11 Medical treatment)
3.6 Cellular biology (Part of: 3 Laboratory methods)
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
