SOX2 haploinsufficiency promotes impaired vision at advanced age
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Leire Moreno-Cugnon1, Ander Anasagasti2, Maitane Ezquerra-Inchausti2, Ander Izeta3, Pedro de la Villa4,5, Javier Ruiz-Ederra2,5 and Ander Matheu1,6
1Cellular Oncology Group, Biodonostia Health Research Institute, San Sebastián, Spain
2Sensorial Neurodegeneration Group, Biodonostia Health Research Institute, San Sebastián, Spain
3Tissue Engineering Laboratory, Biodonostia Health Research Institute, San Sebastián, Spain
4Visual Neurophysiology, IRYCIS, University of Alcala, Madrid, Spain
5RETICS OFTARED, Madrid, Spain
6IKERBASQUE, Basque Foundation for Science and CIBERfes, Bilbao, Spain
Ander Matheu, email: [email protected]
Javier Ruiz-Ederra, email: [email protected]
Keywords: Sox2; haploinsufficiency; aging; retina stem cell progenitors; vision loss
Received: July 18, 2018 Accepted: November 01, 2018 Published: November 30, 2018
Age-related vision loss has been associated with degeneration of the retina and decline in Müller glia cell activity. Sox2 is a critical transcription factor for the development and maintenance of the mammalian retina. Here we determined the role of Sox2 in retinal aging. We observed a decline in the number of Sox2-positive Müller, amacrine and ganglion cells with age. We also explored the impact of Sox2 haploinsufficiency (Sox2GFP) on the activity of Müller glia cells and vision loss with age. Reduction of Sox2-positive cells promoted impaired Müller glia cell function at advanced age of Sox2GFP. These findings correlated with a significant decline in electroretinographic response in Sox2 haploinsufficient mice. Together, these results indicate that Sox2 is required for the maintenance of the transmission of visual information from cones and rods, and suggest that decline in Sox2 expression is responsible for retinal cell aging and age-related vision loss.
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