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dc.contributor.authorZieger, Marina
dc.contributor.authorPunzo, Claudio
dc.date2022-08-11T08:09:44.000
dc.date.accessioned2022-08-23T16:41:43Z
dc.date.available2022-08-23T16:41:43Z
dc.date.issued2016-03-01
dc.date.submitted2016-05-18
dc.identifier.citationOncotarget. 2016 Mar 1;7(9):9620-33. doi: 10.18632/oncotarget.7330. <a href="http://dx.doi.org/10.18632/oncotarget.7330">Link to article on publisher's site</a>
dc.identifier.issn1949-2553 (Linking)
dc.identifier.doi10.18632/oncotarget.7330
dc.identifier.pmid26883199
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39943
dc.description.abstractAge-related macular degeneration (AMD) is characterized by malfunction and loss of retinal-pigmented epithelium (RPE) cells. Because the RPE transfers nutrients from the choriocapillaris to photoreceptor (PR), PRs are affected as well. Geographic atrophy (GA) is an advanced form of AMD characterized by severe vision impairment due to RPE loss over large areas. Currently there is no treatment to delay the degeneration of nutrient deprived PRs once RPE cells die. Here we show that cell-autonomous activation of the key regulator of cell metabolism, the kinase mammalian target of rapamycin complex 1 (mTORC1), delays PR death in the sodium iodate induced model of RPE atrophy. Consistent with this finding loss of mTORC1 in cones accelerates cone death as cones fail to balance demand with supply. Interestingly, promoting rod survival does not promote cone survival in this model of RPE atrophy as both, rods and cones suffer from a sick and dying RPE. The findings suggest that activation of metabolic genes downstream of mTORC1 can serve as a strategy to prolong PR survival when RPE cells malfunction or die.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26883199&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsAll Oncotarget site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/
dc.subjectAMD
dc.subjectGerotarget
dc.subjectcone degeneration
dc.subjectgeographic atrophy
dc.subjectmTORC1
dc.subjectrod degeneration
dc.subjectCellular and Molecular Physiology
dc.subjectEye Diseases
dc.subjectOphthalmology
dc.titleImproved cell metabolism prolongs photoreceptor survival upon retinal-pigmented epithelium loss in the sodium iodate induced model of geographic atrophy
dc.typeJournal Article
dc.source.journaltitleOncotarget
dc.source.volume7
dc.source.issue9
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3757&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2752
dc.identifier.contextkey8614704
refterms.dateFOA2022-08-23T16:41:44Z
html.description.abstract<p>Age-related macular degeneration (AMD) is characterized by malfunction and loss of retinal-pigmented epithelium (RPE) cells. Because the RPE transfers nutrients from the choriocapillaris to photoreceptor (PR), PRs are affected as well. Geographic atrophy (GA) is an advanced form of AMD characterized by severe vision impairment due to RPE loss over large areas. Currently there is no treatment to delay the degeneration of nutrient deprived PRs once RPE cells die. Here we show that cell-autonomous activation of the key regulator of cell metabolism, the kinase mammalian target of rapamycin complex 1 (mTORC1), delays PR death in the sodium iodate induced model of RPE atrophy. Consistent with this finding loss of mTORC1 in cones accelerates cone death as cones fail to balance demand with supply. Interestingly, promoting rod survival does not promote cone survival in this model of RPE atrophy as both, rods and cones suffer from a sick and dying RPE. The findings suggest that activation of metabolic genes downstream of mTORC1 can serve as a strategy to prolong PR survival when RPE cells malfunction or die.</p>
dc.identifier.submissionpathoapubs/2752
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentGene Therapy Center
dc.contributor.departmentDepartment of Ophthalmology
dc.source.pages9620-33


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All Oncotarget site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
Except where otherwise noted, this item's license is described as All Oncotarget site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.