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Collapsin Response Mediator Protein-2-induced Retinal Ischemic Injury in a Novel Mice Model of Ocular Ischemia Syndrome

BACKGROUND: Collapsin response mediator protein-2 (CRMP2) has been shown to be involved in ischemia/hypoxia (IH) injury. We determined whether CRMP2 modulates ischemic injury in the retinal of Ocular ischemic syndrome (OIS). This study was to explore the molecular mechanisms underlying OIS in a nove...

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Autores principales: Wang, Yu, Wang, Xiao-Lei, Xie, Guo-Li, Li, Hong-Yang, Wang, Yan-Ling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5455045/
https://www.ncbi.nlm.nih.gov/pubmed/28524835
http://dx.doi.org/10.4103/0366-6999.206340
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author Wang, Yu
Wang, Xiao-Lei
Xie, Guo-Li
Li, Hong-Yang
Wang, Yan-Ling
author_facet Wang, Yu
Wang, Xiao-Lei
Xie, Guo-Li
Li, Hong-Yang
Wang, Yan-Ling
author_sort Wang, Yu
collection PubMed
description BACKGROUND: Collapsin response mediator protein-2 (CRMP2) has been shown to be involved in ischemia/hypoxia (IH) injury. We determined whether CRMP2 modulates ischemic injury in the retinal of Ocular ischemic syndrome (OIS). This study was to explore the molecular mechanisms underlying OIS in a novel mice model. METHODS: Experiments were performed on adult male C57/BL6 mice that received bilateral internal carotid arteries ligation for 1, 2, or 4 weeks. The mice received injection of calpeptin group before occlusion for 4 weeks or not. The expression of CRMP2 in the retinal was examined by western blotting (WB) analysis and immunohistochemical analysis (IHC). The effects of ischemic injury on retinal were evaluated by fundus examination, fundus fluorescein angiography, electroretinogram, cell counting of retinal ganglion cell (RGC), and measurement of the thickness of the retina. RESULTS: The veins dilated after chronic ischemia. In the electroretinography, the amplitudes of a- and b-waves kept diminishing in an ischemia time-dependent manner. Moreover, the tail vein-retinal circulation time prolonged in the 1- and 2-week group. In comparison, thickness of the retina decreased gradually with the ischemia time elapsed. WB analysis showed the CRMP2 and p-CRMP2 levels decreased in the 2- and 4-week groups. The results of IHC analysis were compatible with our results of WB. The loss of RGCs, decrease of the total reaction time and reduction of CRMP2 was alleviated by intravitreal injection of calpeptin. CONCLUSIONS: These results revealed that bilateral ligation of the internal carotid artery causes retinal ischemia in mice. Moreover, CRMP2 might play a pivotal role during the ischemic injury in the retina and inhibit the cleavage of CRMP2 can ameliorate the IH injury.
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spelling pubmed-54550452017-06-06 Collapsin Response Mediator Protein-2-induced Retinal Ischemic Injury in a Novel Mice Model of Ocular Ischemia Syndrome Wang, Yu Wang, Xiao-Lei Xie, Guo-Li Li, Hong-Yang Wang, Yan-Ling Chin Med J (Engl) Original Article BACKGROUND: Collapsin response mediator protein-2 (CRMP2) has been shown to be involved in ischemia/hypoxia (IH) injury. We determined whether CRMP2 modulates ischemic injury in the retinal of Ocular ischemic syndrome (OIS). This study was to explore the molecular mechanisms underlying OIS in a novel mice model. METHODS: Experiments were performed on adult male C57/BL6 mice that received bilateral internal carotid arteries ligation for 1, 2, or 4 weeks. The mice received injection of calpeptin group before occlusion for 4 weeks or not. The expression of CRMP2 in the retinal was examined by western blotting (WB) analysis and immunohistochemical analysis (IHC). The effects of ischemic injury on retinal were evaluated by fundus examination, fundus fluorescein angiography, electroretinogram, cell counting of retinal ganglion cell (RGC), and measurement of the thickness of the retina. RESULTS: The veins dilated after chronic ischemia. In the electroretinography, the amplitudes of a- and b-waves kept diminishing in an ischemia time-dependent manner. Moreover, the tail vein-retinal circulation time prolonged in the 1- and 2-week group. In comparison, thickness of the retina decreased gradually with the ischemia time elapsed. WB analysis showed the CRMP2 and p-CRMP2 levels decreased in the 2- and 4-week groups. The results of IHC analysis were compatible with our results of WB. The loss of RGCs, decrease of the total reaction time and reduction of CRMP2 was alleviated by intravitreal injection of calpeptin. CONCLUSIONS: These results revealed that bilateral ligation of the internal carotid artery causes retinal ischemia in mice. Moreover, CRMP2 might play a pivotal role during the ischemic injury in the retina and inhibit the cleavage of CRMP2 can ameliorate the IH injury. Medknow Publications & Media Pvt Ltd 2017-06-05 /pmc/articles/PMC5455045/ /pubmed/28524835 http://dx.doi.org/10.4103/0366-6999.206340 Text en Copyright: © 2017 Chinese Medical Journal http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
spellingShingle Original Article
Wang, Yu
Wang, Xiao-Lei
Xie, Guo-Li
Li, Hong-Yang
Wang, Yan-Ling
Collapsin Response Mediator Protein-2-induced Retinal Ischemic Injury in a Novel Mice Model of Ocular Ischemia Syndrome
title Collapsin Response Mediator Protein-2-induced Retinal Ischemic Injury in a Novel Mice Model of Ocular Ischemia Syndrome
title_full Collapsin Response Mediator Protein-2-induced Retinal Ischemic Injury in a Novel Mice Model of Ocular Ischemia Syndrome
title_fullStr Collapsin Response Mediator Protein-2-induced Retinal Ischemic Injury in a Novel Mice Model of Ocular Ischemia Syndrome
title_full_unstemmed Collapsin Response Mediator Protein-2-induced Retinal Ischemic Injury in a Novel Mice Model of Ocular Ischemia Syndrome
title_short Collapsin Response Mediator Protein-2-induced Retinal Ischemic Injury in a Novel Mice Model of Ocular Ischemia Syndrome
title_sort collapsin response mediator protein-2-induced retinal ischemic injury in a novel mice model of ocular ischemia syndrome
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5455045/
https://www.ncbi.nlm.nih.gov/pubmed/28524835
http://dx.doi.org/10.4103/0366-6999.206340
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