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Sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling

Dysfunction of protein trafficking has been intensively associated with neurological diseases, including neurodegeneration, but whether and how protein transport contributes to oligodendrocyte (OL) maturation and myelin repair in white matter injury remains unclear. ER-to-Golgi trafficking of newly...

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Autores principales: Liu, Zhixiong, Yan, Minbiao, Lei, Wanying, Jiang, Rencai, Dai, Wenxiu, Chen, Jialin, Wang, Chaomeng, Li, Li, Wu, Mei, Nian, Ximing, Li, Daopeng, Sun, Di, Lv, Xiaoqi, Wang, Chaoying, Xie, Changchuan, Yao, Luming, Wu, Caiming, Hu, Jin, Xiao, Naian, Mo, Wei, Wang, Zhanxiang, Zhang, Liang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Clinical Investigation 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8970680/
https://www.ncbi.nlm.nih.gov/pubmed/35143418
http://dx.doi.org/10.1172/JCI155096
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author Liu, Zhixiong
Yan, Minbiao
Lei, Wanying
Jiang, Rencai
Dai, Wenxiu
Chen, Jialin
Wang, Chaomeng
Li, Li
Wu, Mei
Nian, Ximing
Li, Daopeng
Sun, Di
Lv, Xiaoqi
Wang, Chaoying
Xie, Changchuan
Yao, Luming
Wu, Caiming
Hu, Jin
Xiao, Naian
Mo, Wei
Wang, Zhanxiang
Zhang, Liang
author_facet Liu, Zhixiong
Yan, Minbiao
Lei, Wanying
Jiang, Rencai
Dai, Wenxiu
Chen, Jialin
Wang, Chaomeng
Li, Li
Wu, Mei
Nian, Ximing
Li, Daopeng
Sun, Di
Lv, Xiaoqi
Wang, Chaoying
Xie, Changchuan
Yao, Luming
Wu, Caiming
Hu, Jin
Xiao, Naian
Mo, Wei
Wang, Zhanxiang
Zhang, Liang
author_sort Liu, Zhixiong
collection PubMed
description Dysfunction of protein trafficking has been intensively associated with neurological diseases, including neurodegeneration, but whether and how protein transport contributes to oligodendrocyte (OL) maturation and myelin repair in white matter injury remains unclear. ER-to-Golgi trafficking of newly synthesized proteins is mediated by coat protein complex II (COPII). Here, we demonstrate that the COPII component Sec13 was essential for OL differentiation and postnatal myelination. Ablation of Sec13 in the OL lineage prevented OPC differentiation and inhibited myelination and remyelination after demyelinating injury in the central nervous system (CNS), while improving protein trafficking by tauroursodeoxycholic acid (TUDCA) or ectopic expression of COPII components accelerated myelination. COPII components were upregulated in OL lineage cells after demyelinating injury. Loss of Sec13 altered the secretome of OLs and inhibited the secretion of pleiotrophin (PTN), which was found to function as an autocrine factor to promote OL differentiation and myelin repair. These data suggest that Sec13-dependent protein transport is essential for OL differentiation and that Sec13-mediated PTN autocrine signaling is required for proper myelination and remyelination.
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spelling pubmed-89706802022-04-06 Sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling Liu, Zhixiong Yan, Minbiao Lei, Wanying Jiang, Rencai Dai, Wenxiu Chen, Jialin Wang, Chaomeng Li, Li Wu, Mei Nian, Ximing Li, Daopeng Sun, Di Lv, Xiaoqi Wang, Chaoying Xie, Changchuan Yao, Luming Wu, Caiming Hu, Jin Xiao, Naian Mo, Wei Wang, Zhanxiang Zhang, Liang J Clin Invest Research Article Dysfunction of protein trafficking has been intensively associated with neurological diseases, including neurodegeneration, but whether and how protein transport contributes to oligodendrocyte (OL) maturation and myelin repair in white matter injury remains unclear. ER-to-Golgi trafficking of newly synthesized proteins is mediated by coat protein complex II (COPII). Here, we demonstrate that the COPII component Sec13 was essential for OL differentiation and postnatal myelination. Ablation of Sec13 in the OL lineage prevented OPC differentiation and inhibited myelination and remyelination after demyelinating injury in the central nervous system (CNS), while improving protein trafficking by tauroursodeoxycholic acid (TUDCA) or ectopic expression of COPII components accelerated myelination. COPII components were upregulated in OL lineage cells after demyelinating injury. Loss of Sec13 altered the secretome of OLs and inhibited the secretion of pleiotrophin (PTN), which was found to function as an autocrine factor to promote OL differentiation and myelin repair. These data suggest that Sec13-dependent protein transport is essential for OL differentiation and that Sec13-mediated PTN autocrine signaling is required for proper myelination and remyelination. American Society for Clinical Investigation 2022-04-01 2022-04-01 /pmc/articles/PMC8970680/ /pubmed/35143418 http://dx.doi.org/10.1172/JCI155096 Text en © 2022 Liu et al. https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Article
Liu, Zhixiong
Yan, Minbiao
Lei, Wanying
Jiang, Rencai
Dai, Wenxiu
Chen, Jialin
Wang, Chaomeng
Li, Li
Wu, Mei
Nian, Ximing
Li, Daopeng
Sun, Di
Lv, Xiaoqi
Wang, Chaoying
Xie, Changchuan
Yao, Luming
Wu, Caiming
Hu, Jin
Xiao, Naian
Mo, Wei
Wang, Zhanxiang
Zhang, Liang
Sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling
title Sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling
title_full Sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling
title_fullStr Sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling
title_full_unstemmed Sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling
title_short Sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling
title_sort sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8970680/
https://www.ncbi.nlm.nih.gov/pubmed/35143418
http://dx.doi.org/10.1172/JCI155096
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