The temporal topography of the N-Methyl- N-nitrosourea induced photoreceptor degeneration in mouse retina

Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases characterized by the progressive photoreceptors apoptosis. The N-Methyl- N-nitrosourea (MNU) is an alkylating toxicant which could induce photoreceptor apoptosis resembling that of the hereditary RP. However, the detailed p...

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Main Authors: Tao, Ye, Chen, Tao, Fang, Wei, Peng, Guanghua, Wang, liqiang, Qin, Limin, Liu, Bei, Fei Huang, Yi
Formato: Artigo
Idioma:Inglês
Publicado: Nature Publishing Group 2015
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Acceso en liña:https://ncbi.nlm.nih.gov/pmc/articles/PMC4685653/
https://ncbi.nlm.nih.gov/pubmed/26685797
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/srep18612
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spelling pubmed-46856532015-12-30 The temporal topography of the N-Methyl- N-nitrosourea induced photoreceptor degeneration in mouse retina Tao, Ye Chen, Tao Fang, Wei Peng, Guanghua Wang, liqiang Qin, Limin Liu, Bei Fei Huang, Yi Sci Rep Article Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases characterized by the progressive photoreceptors apoptosis. The N-Methyl- N-nitrosourea (MNU) is an alkylating toxicant which could induce photoreceptor apoptosis resembling that of the hereditary RP. However, the detailed process pattern of this degeneration remains poorly characterized. We systemically explored the topography of the photoreceptor degeneration in the MNU treated mouse, and related these spatial data with the time-dependent characteristics of retinal pathology. These temporal topographic data delineated sequential scenes of the progressive photoreceptor degeneration in the MNU treated retinas: focal photoreceptors showed different vulnerabilities to the MNU toxicity and displayed a distinctive spatial- and time-dependent progression. Moreover, the positional asymmetry between the retinal quadrants firstly provided instructive information about the unique toxicology properties of the MNU. Further mechanism study suggested that the up-regulation of Bax and Calpain-2, rather than the Caspase-3, should be responsible for the asymmetry in the MNU induced photoreceptor degeneration. Together with the comparative sensitivities to the neurotoxicity of MNU between two photoreceptor populations, these topographic data would facilitate the standardization of analytic parameters related to the MNU induced RP model, and enhance its application in the therapeutic explorations of human RP. Nature Publishing Group 2015-12-21 /pmc/articles/PMC4685653/ /pubmed/26685797 http://dx.doi.org/10.1038/srep18612 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
institution US NLM
collection PubMed Central
language Inglês
format Artigo
topic Article
spellingShingle Article
Tao, Ye
Chen, Tao
Fang, Wei
Peng, Guanghua
Wang, liqiang
Qin, Limin
Liu, Bei
Fei Huang, Yi
The temporal topography of the N-Methyl- N-nitrosourea induced photoreceptor degeneration in mouse retina
description Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases characterized by the progressive photoreceptors apoptosis. The N-Methyl- N-nitrosourea (MNU) is an alkylating toxicant which could induce photoreceptor apoptosis resembling that of the hereditary RP. However, the detailed process pattern of this degeneration remains poorly characterized. We systemically explored the topography of the photoreceptor degeneration in the MNU treated mouse, and related these spatial data with the time-dependent characteristics of retinal pathology. These temporal topographic data delineated sequential scenes of the progressive photoreceptor degeneration in the MNU treated retinas: focal photoreceptors showed different vulnerabilities to the MNU toxicity and displayed a distinctive spatial- and time-dependent progression. Moreover, the positional asymmetry between the retinal quadrants firstly provided instructive information about the unique toxicology properties of the MNU. Further mechanism study suggested that the up-regulation of Bax and Calpain-2, rather than the Caspase-3, should be responsible for the asymmetry in the MNU induced photoreceptor degeneration. Together with the comparative sensitivities to the neurotoxicity of MNU between two photoreceptor populations, these topographic data would facilitate the standardization of analytic parameters related to the MNU induced RP model, and enhance its application in the therapeutic explorations of human RP.
author Tao, Ye
Chen, Tao
Fang, Wei
Peng, Guanghua
Wang, liqiang
Qin, Limin
Liu, Bei
Fei Huang, Yi
author_facet Tao, Ye
Chen, Tao
Fang, Wei
Peng, Guanghua
Wang, liqiang
Qin, Limin
Liu, Bei
Fei Huang, Yi
author_sort Tao, Ye
title The temporal topography of the N-Methyl- N-nitrosourea induced photoreceptor degeneration in mouse retina
title_short The temporal topography of the N-Methyl- N-nitrosourea induced photoreceptor degeneration in mouse retina
title_full The temporal topography of the N-Methyl- N-nitrosourea induced photoreceptor degeneration in mouse retina
title_fullStr The temporal topography of the N-Methyl- N-nitrosourea induced photoreceptor degeneration in mouse retina
title_full_unstemmed The temporal topography of the N-Methyl- N-nitrosourea induced photoreceptor degeneration in mouse retina
title_sort temporal topography of the n-methyl- n-nitrosourea induced photoreceptor degeneration in mouse retina
publisher Nature Publishing Group
container_title Sci Rep
publishDate 2015
url https://ncbi.nlm.nih.gov/pmc/articles/PMC4685653/
https://ncbi.nlm.nih.gov/pubmed/26685797
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/srep18612
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