title: Mitochondrial Uncoupling Protein 2 (UCP2) Regulates Retinal Ganglion Cell Number and Survival.
abstract: In the brain, mitochondrial uncoupling protein 2 (UCP2) has emerged as a stress signal associated with neuronal survival. In the retina, UCP2 is expressed primarily by retinal ganglion cells. Here, we investigated the functional relevance of UCP2 in the mouse retina. Increased expression of UCP2 significantly reduced apoptosis during the critical developmental period resulting in elevated numbers of retinal ganglion cells in the adult. Elevated UCP2 levels also protected against excitotoxic cell death induced by intraocular injection of either NMDA or kainic acid. In monolayer cultures of retinal cells, elevated UCP2 levels increased cell survival and rendered the cells independent of the survival-promoting effects of the neurotrophic factors BDNF and CNTF. Taken together, these data implicate UCP2 as an important regulator of retinal neuron survival both during development and in adult animals.
authors: Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, CT, 06510, USA. cjb30@psu.edu.|Department of Neurobiology, Yale University School of Medicine, New Haven, CT, 06510, USA. cjb30@psu.edu.|Department of Neural and Behavioral Science, Penn State University College of Medicine, H109, 500 University Drive, Hershey, PA, 17033, USA. cjb30@psu.edu.
authors: Colin J
authors: CJ
authors: Barnstable
authors: Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, CT, 06510, USA.
authors: Rajini
authors: R
authors: Reddy
authors: Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, CT, 06510, USA.|Department of Neural and Behavioral Science, Penn State University College of Medicine, H109, 500 University Drive, Hershey, PA, 17033, USA.
authors: Hong
authors: H
authors: Li
authors: Department of Neurobiology, Yale University School of Medicine, New Haven, CT, 06510, USA.|Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, 06510, USA.|Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT, 06510, USA.
authors: Tamas L
authors: TL
authors: Horvath
mesh_terms: D000818:Animals; D017209:Apoptosis; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D002470:Cell Survival; D002478:Cells, Cultured; D020934:Ciliary Neurotrophic Factor / Q000378:metabolism; D007608:Kainic Acid / Q000633:toxicity; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016202:N-Methylaspartate / Q000633:toxicity; D055495:Neurogenesis; D012165:Retinal Ganglion Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000071246:Uncoupling Protein 2 / Q000235:genetics / Q000378:metabolism*
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D020934:Ciliary Neurotrophic Factor; C000604390:Ucp2 protein, mouse; D000071246:Uncoupling Protein 2; D016202:N-Methylaspartate; D007608:Kainic Acid
keywords: Development; Excitotoxicity; Neuroprotection; Programmed cell death; Reactive oxygen species; Retinal ganglion cell