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Retinol dehydrogenase 13 protects the mouse retina from acute light damage

PURPOSE: To investigate whether retinol dehydrogenase 13 (RDH13) can protect the retina from acute light-induced damage. METHODS: We generated Rdh13 knockout mice using molecular biologic methods and assessed the associated morphological and functional changes under room-light conditions by hematoxy...

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Autores principales: Wang, Haiyan, Cui, Xiaofang, Gu, Qing, Chen, Yan, Zhou, Jia, Kuang, Ying, Wang, Zhugang, Xu, Xun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Vision 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3351414/
https://www.ncbi.nlm.nih.gov/pubmed/22605914
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author Wang, Haiyan
Cui, Xiaofang
Gu, Qing
Chen, Yan
Zhou, Jia
Kuang, Ying
Wang, Zhugang
Xu, Xun
author_facet Wang, Haiyan
Cui, Xiaofang
Gu, Qing
Chen, Yan
Zhou, Jia
Kuang, Ying
Wang, Zhugang
Xu, Xun
author_sort Wang, Haiyan
collection PubMed
description PURPOSE: To investigate whether retinol dehydrogenase 13 (RDH13) can protect the retina from acute light-induced damage. METHODS: We generated Rdh13 knockout mice using molecular biologic methods and assessed the associated morphological and functional changes under room-light conditions by hematoxylin-eosin (H&E), transmission electron microscopy (TEM), and scotopic electroretinography. Then, the light-damage model was established by exposure to diffuse white light (3,000 lx) for 48 h. Twenty-four h after light exposure, H&E was used for the histological evaluation. The thickness of the outer-plus-inner-segment and the outer nuclear layer was measured on sections parallel to the vertical meridian of the eye. An electroretinography test was performed to assess the functional change. Furthermore, the impairment of mitochondria was detected by TEM. Finally, the expression of cytochrome c (CytC) and other apoptosis-related proteins was detected by western blot. RESULTS: We found that there was no obvious difference in phenotype or function between Rdh13 knockout and wild-type mice. In Rdh13(−/−) mice subjected to intense light exposure, the photoreceptor outer-plus-inner-segment and outer nuclear layer were dramatically shorter, and the amplitudes of a- and b-waves under scotopic conditions were significantly attenuated. Distinctly swollen mitochondria with disrupted cristae were observed in the photoreceptor inner segments of Rdh13(−/−) mice. Increased expression levels of CytC, CytC-responsive apoptosis proteinase activating factor-1 (Apaf-1) and caspases 3, and other mitochondria apoptosis-related genes (nuclear factor-kappa B P65 [P65] and B-cell lymphoma 2-associated X protein [Bax]) were observed in Rdh13(−/−) mice. CONCLUSIONS: Rdh13 can protect the retina against acute light-induced retinopathy. The mechanism may involve inhibition of the mitochondrial apoptosis pathway.
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spelling pubmed-33514142012-05-17 Retinol dehydrogenase 13 protects the mouse retina from acute light damage Wang, Haiyan Cui, Xiaofang Gu, Qing Chen, Yan Zhou, Jia Kuang, Ying Wang, Zhugang Xu, Xun Mol Vis Letter to Editor PURPOSE: To investigate whether retinol dehydrogenase 13 (RDH13) can protect the retina from acute light-induced damage. METHODS: We generated Rdh13 knockout mice using molecular biologic methods and assessed the associated morphological and functional changes under room-light conditions by hematoxylin-eosin (H&E), transmission electron microscopy (TEM), and scotopic electroretinography. Then, the light-damage model was established by exposure to diffuse white light (3,000 lx) for 48 h. Twenty-four h after light exposure, H&E was used for the histological evaluation. The thickness of the outer-plus-inner-segment and the outer nuclear layer was measured on sections parallel to the vertical meridian of the eye. An electroretinography test was performed to assess the functional change. Furthermore, the impairment of mitochondria was detected by TEM. Finally, the expression of cytochrome c (CytC) and other apoptosis-related proteins was detected by western blot. RESULTS: We found that there was no obvious difference in phenotype or function between Rdh13 knockout and wild-type mice. In Rdh13(−/−) mice subjected to intense light exposure, the photoreceptor outer-plus-inner-segment and outer nuclear layer were dramatically shorter, and the amplitudes of a- and b-waves under scotopic conditions were significantly attenuated. Distinctly swollen mitochondria with disrupted cristae were observed in the photoreceptor inner segments of Rdh13(−/−) mice. Increased expression levels of CytC, CytC-responsive apoptosis proteinase activating factor-1 (Apaf-1) and caspases 3, and other mitochondria apoptosis-related genes (nuclear factor-kappa B P65 [P65] and B-cell lymphoma 2-associated X protein [Bax]) were observed in Rdh13(−/−) mice. CONCLUSIONS: Rdh13 can protect the retina against acute light-induced retinopathy. The mechanism may involve inhibition of the mitochondrial apoptosis pathway. Molecular Vision 2012-04-24 /pmc/articles/PMC3351414/ /pubmed/22605914 Text en Copyright © 2012 Molecular Vision. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Letter to Editor
Wang, Haiyan
Cui, Xiaofang
Gu, Qing
Chen, Yan
Zhou, Jia
Kuang, Ying
Wang, Zhugang
Xu, Xun
Retinol dehydrogenase 13 protects the mouse retina from acute light damage
title Retinol dehydrogenase 13 protects the mouse retina from acute light damage
title_full Retinol dehydrogenase 13 protects the mouse retina from acute light damage
title_fullStr Retinol dehydrogenase 13 protects the mouse retina from acute light damage
title_full_unstemmed Retinol dehydrogenase 13 protects the mouse retina from acute light damage
title_short Retinol dehydrogenase 13 protects the mouse retina from acute light damage
title_sort retinol dehydrogenase 13 protects the mouse retina from acute light damage
topic Letter to Editor
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3351414/
https://www.ncbi.nlm.nih.gov/pubmed/22605914
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