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The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders

This study aimed to investigate the expression of autophagy-related proteins in a mouse model of neuromyelitis optica (NMO). Mice were assigned to one of four groups: an animal experimental model group (NMO-EAE group, given with exogenous IL-17A), Interleukin-17 monoclonal antibody intervention grou...

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Autores principales: Guo, Hong-Liang, Shen, Xiao-Ran, Liang, Xiao-Ting, Li, Ling-Zhou
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9995123/
https://www.ncbi.nlm.nih.gov/pubmed/36694421
http://dx.doi.org/10.1080/21655979.2022.2084273
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author Guo, Hong-Liang
Shen, Xiao-Ran
Liang, Xiao-Ting
Li, Ling-Zhou
author_facet Guo, Hong-Liang
Shen, Xiao-Ran
Liang, Xiao-Ting
Li, Ling-Zhou
author_sort Guo, Hong-Liang
collection PubMed
description This study aimed to investigate the expression of autophagy-related proteins in a mouse model of neuromyelitis optica (NMO). Mice were assigned to one of four groups: an animal experimental model group (NMO-EAE group, given with exogenous IL-17A), Interleukin-17 monoclonal antibody intervention group (NMO-EAE_0IL17inb), No exogenous interleukin-17 enhanced immune intervention group (NMO-EAE_0IL17), and a control group. Behavioral scores were assessed in each group, and the protein expressions of sequestosome 1 (P62), Beclin-1, the mammalian target of rapamycin (mTOR), phosphoinositide 3-kinase (PI3K-I), and LC3II/LC3I were detected using Western blotting. In the NMO-EAE_0IL17 group, the expression of Beclin-1 decreased, the LC3II/LC3I ratio was lower, and the expressions of P62, mTOR, and PI3K-I increased; after administration of IL-17A inhibitor into the brain tissue, however, the expression of Beclin-1 increased significantly, along with the LC3II/LC3I ratio, while the expressions of P62, mTOR and PI3K-I protein decreased significantly. In terms of behavioral scores, the scores of optic neuritis and myelitis were more serious, onset occurred earlier and the progress was faster, after the administration of IL-17A. In the mechanism of NMO animal model, IL-17A may regulate autophagy and affect the disease process through the activation of the PI3K–mTOR signaling pathway.
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spelling pubmed-99951232023-03-09 The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders Guo, Hong-Liang Shen, Xiao-Ran Liang, Xiao-Ting Li, Ling-Zhou Bioengineered Research Paper This study aimed to investigate the expression of autophagy-related proteins in a mouse model of neuromyelitis optica (NMO). Mice were assigned to one of four groups: an animal experimental model group (NMO-EAE group, given with exogenous IL-17A), Interleukin-17 monoclonal antibody intervention group (NMO-EAE_0IL17inb), No exogenous interleukin-17 enhanced immune intervention group (NMO-EAE_0IL17), and a control group. Behavioral scores were assessed in each group, and the protein expressions of sequestosome 1 (P62), Beclin-1, the mammalian target of rapamycin (mTOR), phosphoinositide 3-kinase (PI3K-I), and LC3II/LC3I were detected using Western blotting. In the NMO-EAE_0IL17 group, the expression of Beclin-1 decreased, the LC3II/LC3I ratio was lower, and the expressions of P62, mTOR, and PI3K-I increased; after administration of IL-17A inhibitor into the brain tissue, however, the expression of Beclin-1 increased significantly, along with the LC3II/LC3I ratio, while the expressions of P62, mTOR and PI3K-I protein decreased significantly. In terms of behavioral scores, the scores of optic neuritis and myelitis were more serious, onset occurred earlier and the progress was faster, after the administration of IL-17A. In the mechanism of NMO animal model, IL-17A may regulate autophagy and affect the disease process through the activation of the PI3K–mTOR signaling pathway. Taylor & Francis 2023-01-24 /pmc/articles/PMC9995123/ /pubmed/36694421 http://dx.doi.org/10.1080/21655979.2022.2084273 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) ), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Guo, Hong-Liang
Shen, Xiao-Ran
Liang, Xiao-Ting
Li, Ling-Zhou
The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders
title The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders
title_full The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders
title_fullStr The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders
title_full_unstemmed The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders
title_short The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders
title_sort role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9995123/
https://www.ncbi.nlm.nih.gov/pubmed/36694421
http://dx.doi.org/10.1080/21655979.2022.2084273
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