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Myosin 1f-mediated activation of microglia contributes to the photoreceptor degeneration in a mouse model of retinal detachment

Photoreceptor death and neurodegeneration is the leading cause of irreversible vision loss. The inflammatory response of microglia plays an important role in the process of neurodegeneration. In this study, we chose retinal detachment as the model of photoreceptor degeneration. We found Myosin 1f wa...

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Autores principales: Wang, Yimin, Zhao, Xiaohuan, Gao, Min, Wan, Xiaoling, Guo, Yinong, Qu, Yingying, Chen, Yuhong, Li, Tong, Liu, Haiyun, Jiang, Mei, Wang, Feng, Sun, Xiaodong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8502177/
https://www.ncbi.nlm.nih.gov/pubmed/34628463
http://dx.doi.org/10.1038/s41419-021-03983-3
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author Wang, Yimin
Zhao, Xiaohuan
Gao, Min
Wan, Xiaoling
Guo, Yinong
Qu, Yingying
Chen, Yuhong
Li, Tong
Liu, Haiyun
Jiang, Mei
Wang, Feng
Sun, Xiaodong
author_facet Wang, Yimin
Zhao, Xiaohuan
Gao, Min
Wan, Xiaoling
Guo, Yinong
Qu, Yingying
Chen, Yuhong
Li, Tong
Liu, Haiyun
Jiang, Mei
Wang, Feng
Sun, Xiaodong
author_sort Wang, Yimin
collection PubMed
description Photoreceptor death and neurodegeneration is the leading cause of irreversible vision loss. The inflammatory response of microglia plays an important role in the process of neurodegeneration. In this study, we chose retinal detachment as the model of photoreceptor degeneration. We found Myosin 1f was upregulated after retinal detachment, and it was specifically expressed in microglia. Deficiency of myosin 1f protected against photoreceptor apoptosis by inhibiting microglia activation. The elimination of microglia can abolish the protective effect of myosin 1f deficiency. After stimulation by LPS, microglia with myosin 1f deficiency showed downregulation of the MAPK and AKT pathways. Our results demonstrated that myosin 1f plays a crucial role in microglia-induced neuroinflammation after retinal injury and photoreceptor degeneration by regulating two classic inflammatory pathways and thereby decreasing the expression of inflammatory cytokines. Knockout of myosin 1f reduces the intensity of the immune response and prevents cell death of photoreceptor, suggesting that myosin 1f can be inhibited to prevent a decline in visual acuity after retinal detachment.
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spelling pubmed-85021772021-10-22 Myosin 1f-mediated activation of microglia contributes to the photoreceptor degeneration in a mouse model of retinal detachment Wang, Yimin Zhao, Xiaohuan Gao, Min Wan, Xiaoling Guo, Yinong Qu, Yingying Chen, Yuhong Li, Tong Liu, Haiyun Jiang, Mei Wang, Feng Sun, Xiaodong Cell Death Dis Article Photoreceptor death and neurodegeneration is the leading cause of irreversible vision loss. The inflammatory response of microglia plays an important role in the process of neurodegeneration. In this study, we chose retinal detachment as the model of photoreceptor degeneration. We found Myosin 1f was upregulated after retinal detachment, and it was specifically expressed in microglia. Deficiency of myosin 1f protected against photoreceptor apoptosis by inhibiting microglia activation. The elimination of microglia can abolish the protective effect of myosin 1f deficiency. After stimulation by LPS, microglia with myosin 1f deficiency showed downregulation of the MAPK and AKT pathways. Our results demonstrated that myosin 1f plays a crucial role in microglia-induced neuroinflammation after retinal injury and photoreceptor degeneration by regulating two classic inflammatory pathways and thereby decreasing the expression of inflammatory cytokines. Knockout of myosin 1f reduces the intensity of the immune response and prevents cell death of photoreceptor, suggesting that myosin 1f can be inhibited to prevent a decline in visual acuity after retinal detachment. Nature Publishing Group UK 2021-10-09 /pmc/articles/PMC8502177/ /pubmed/34628463 http://dx.doi.org/10.1038/s41419-021-03983-3 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Wang, Yimin
Zhao, Xiaohuan
Gao, Min
Wan, Xiaoling
Guo, Yinong
Qu, Yingying
Chen, Yuhong
Li, Tong
Liu, Haiyun
Jiang, Mei
Wang, Feng
Sun, Xiaodong
Myosin 1f-mediated activation of microglia contributes to the photoreceptor degeneration in a mouse model of retinal detachment
title Myosin 1f-mediated activation of microglia contributes to the photoreceptor degeneration in a mouse model of retinal detachment
title_full Myosin 1f-mediated activation of microglia contributes to the photoreceptor degeneration in a mouse model of retinal detachment
title_fullStr Myosin 1f-mediated activation of microglia contributes to the photoreceptor degeneration in a mouse model of retinal detachment
title_full_unstemmed Myosin 1f-mediated activation of microglia contributes to the photoreceptor degeneration in a mouse model of retinal detachment
title_short Myosin 1f-mediated activation of microglia contributes to the photoreceptor degeneration in a mouse model of retinal detachment
title_sort myosin 1f-mediated activation of microglia contributes to the photoreceptor degeneration in a mouse model of retinal detachment
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8502177/
https://www.ncbi.nlm.nih.gov/pubmed/34628463
http://dx.doi.org/10.1038/s41419-021-03983-3
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