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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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Main Authors: Guo, Hong-Liang, Shen, Xiao-Ran, Liang, Xiao-Ting, Li, Ling-Zhou
Format: Article
Published: Taylor and Francis Ltd. 2022
Subjects:
RC Internal medicine
Online Access:http://eprints.um.edu.my/40448/
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spelling my.um.eprints.404482024-11-24T12:55:01Z http://eprints.um.edu.my/40448/ 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 RC Internal medicine 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 and Francis Ltd. 2022-06 Article PeerReviewed Guo, Hong-Liang and Shen, Xiao-Ran and Liang, Xiao-Ting and Li, Ling-Zhou (2022) The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders. Bioengineered, 13 (6). pp. 14329-14338. ISSN 21655979, DOI https://doi.org/10.1080/21655979.2022.2084273 <https://doi.org/10.1080/21655979.2022.2084273>. 10.1080/21655979.2022.2084273
institution Universiti Malaya
building UM Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Malaya
content_source UM Research Repository
url_provider http://eprints.um.edu.my/
topic RC Internal medicine
spellingShingle RC Internal medicine
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
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.
format Article
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
title 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_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_sort role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders
publisher Taylor and Francis Ltd.
publishDate 2022
url http://eprints.um.edu.my/40448/
_version_ 1817841947171094528
score 13.223943

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