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Peritoneal macrophages attenuate retinal ganglion cell survival and neurite outgrowth
Inflammation is a critical pathophysiological process that modulates neuronal survival in the central nervous system after disease or injury. However, the effects and mechanisms of macrophage activation on neuronal survival remain unclear. In the present study, we co-cultured adult Fischer rat retin...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8224139/ https://www.ncbi.nlm.nih.gov/pubmed/33269759 http://dx.doi.org/10.4103/1673-5374.300462 |
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author | Liang, Jia-Jian Liu, Yu-Fen Ng, Tsz Kin Xu, Ci-Yan Zhang, Mingzhi Pang, Chi Pui Cen, Ling-Ping |
author_facet | Liang, Jia-Jian Liu, Yu-Fen Ng, Tsz Kin Xu, Ci-Yan Zhang, Mingzhi Pang, Chi Pui Cen, Ling-Ping |
author_sort | Liang, Jia-Jian |
collection | PubMed |
description | Inflammation is a critical pathophysiological process that modulates neuronal survival in the central nervous system after disease or injury. However, the effects and mechanisms of macrophage activation on neuronal survival remain unclear. In the present study, we co-cultured adult Fischer rat retinas with primary peritoneal macrophages or zymosan-treated peritoneal macrophages for 7 days. Immunofluorescence analysis revealed that peritoneal macrophages reduced retinal ganglion cell survival and neurite outgrowth in the retinal explant compared with the control group. The addition of zymosan to peritoneal macrophages attenuated the survival and neurite outgrowth of retinal ganglion cells. Conditioned media from peritoneal macrophages also reduced retinal ganglion cell survival and neurite outgrowth. This result suggests that secretions from peritoneal macrophages mediate the inhibitory effects of these macrophages. In addition, increased inflammation- and oxidation-related gene expression may be related to the enhanced retinal ganglion cell degeneration caused by zymosan activation. In summary, this study revealed that primary rat peritoneal macrophages attenuated retinal ganglion cell survival and neurite outgrowth, and that macrophage activation further aggravated retinal ganglion cell degeneration. This study was approved by the Animal Ethics Committee of the Joint Shantou International Eye Center of Shantou University and the Chinese University of Hong Kong, Shantou, Guangdong Province, China, on March 11, 2014 (approval no. EC20140311(2)-P01). |
format | Online Article Text |
id | pubmed-8224139 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-82241392021-07-02 Peritoneal macrophages attenuate retinal ganglion cell survival and neurite outgrowth Liang, Jia-Jian Liu, Yu-Fen Ng, Tsz Kin Xu, Ci-Yan Zhang, Mingzhi Pang, Chi Pui Cen, Ling-Ping Neural Regen Res Research Article Inflammation is a critical pathophysiological process that modulates neuronal survival in the central nervous system after disease or injury. However, the effects and mechanisms of macrophage activation on neuronal survival remain unclear. In the present study, we co-cultured adult Fischer rat retinas with primary peritoneal macrophages or zymosan-treated peritoneal macrophages for 7 days. Immunofluorescence analysis revealed that peritoneal macrophages reduced retinal ganglion cell survival and neurite outgrowth in the retinal explant compared with the control group. The addition of zymosan to peritoneal macrophages attenuated the survival and neurite outgrowth of retinal ganglion cells. Conditioned media from peritoneal macrophages also reduced retinal ganglion cell survival and neurite outgrowth. This result suggests that secretions from peritoneal macrophages mediate the inhibitory effects of these macrophages. In addition, increased inflammation- and oxidation-related gene expression may be related to the enhanced retinal ganglion cell degeneration caused by zymosan activation. In summary, this study revealed that primary rat peritoneal macrophages attenuated retinal ganglion cell survival and neurite outgrowth, and that macrophage activation further aggravated retinal ganglion cell degeneration. This study was approved by the Animal Ethics Committee of the Joint Shantou International Eye Center of Shantou University and the Chinese University of Hong Kong, Shantou, Guangdong Province, China, on March 11, 2014 (approval no. EC20140311(2)-P01). Wolters Kluwer - Medknow 2020-11-27 /pmc/articles/PMC8224139/ /pubmed/33269759 http://dx.doi.org/10.4103/1673-5374.300462 Text en Copyright: © 2021 Neural Regeneration Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Research Article Liang, Jia-Jian Liu, Yu-Fen Ng, Tsz Kin Xu, Ci-Yan Zhang, Mingzhi Pang, Chi Pui Cen, Ling-Ping Peritoneal macrophages attenuate retinal ganglion cell survival and neurite outgrowth |
title | Peritoneal macrophages attenuate retinal ganglion cell survival and neurite outgrowth |
title_full | Peritoneal macrophages attenuate retinal ganglion cell survival and neurite outgrowth |
title_fullStr | Peritoneal macrophages attenuate retinal ganglion cell survival and neurite outgrowth |
title_full_unstemmed | Peritoneal macrophages attenuate retinal ganglion cell survival and neurite outgrowth |
title_short | Peritoneal macrophages attenuate retinal ganglion cell survival and neurite outgrowth |
title_sort | peritoneal macrophages attenuate retinal ganglion cell survival and neurite outgrowth |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8224139/ https://www.ncbi.nlm.nih.gov/pubmed/33269759 http://dx.doi.org/10.4103/1673-5374.300462 |
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