Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells

Many genes and signaling pathways have been found to be involved in cellular senescence program. In the present study, we have identified 16 senescence-associated genes by differential proteomic analysis of the normal human diploid fibroblast cell line, TIG-1, and focused on ATP6V0A2. The aim of thi...

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Main Authors: Udono, Miyako, Fujii, Kaoru, Harada, Gakuro, Tsuzuki, Yumi, Kadooka, Keishi, Zhang, Pingbo, Fujii, Hiroshi, Amano, Maho, Nishimura, Shin-Ichiro, Tashiro, Kosuke, Kuhara, Satoru, Katakura, Yoshinori
Format: Online
Language:English
Published: Nature Publishing Group 2015
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4661525/
id pubmed-4661525
recordtype oai_dc
spelling pubmed-46615252015-12-02 Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells Udono, Miyako Fujii, Kaoru Harada, Gakuro Tsuzuki, Yumi Kadooka, Keishi Zhang, Pingbo Fujii, Hiroshi Amano, Maho Nishimura, Shin-Ichiro Tashiro, Kosuke Kuhara, Satoru Katakura, Yoshinori Article Many genes and signaling pathways have been found to be involved in cellular senescence program. In the present study, we have identified 16 senescence-associated genes by differential proteomic analysis of the normal human diploid fibroblast cell line, TIG-1, and focused on ATP6V0A2. The aim of this study is to clarify the role of ATP6V0A2, the causal gene for ARCL2, a syndrome of abnormal glycosylation and impaired Golgi trafficking, in cellular senescence program. Here we showed that ATP6V0A2 is critical for cellular senescence; impaired expression of ATP6V0A2 disperses the Golgi structure and triggers senescence, suggesting that ATP6V0A2 mediates these processes. FITC-lectin staining and glycoblotting revealed significantly different glycosylation structures in presenescent (young) and senescent (old) TIG-1 cells; reducing ATP6V0A2 expression in young TIG-1 cells yielded structures similar to those in old TIG-1 cells. Our results suggest that senescence-associated impaired expression of ATP6V0A2 triggers changes in Golgi structure and glycosylation in old TIG-1 cells, which demonstrates a role of ATP6V0A2 in cellular senescence program. Nature Publishing Group 2015-11-27 /pmc/articles/PMC4661525/ /pubmed/26611489 http://dx.doi.org/10.1038/srep17342 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Udono, Miyako
Fujii, Kaoru
Harada, Gakuro
Tsuzuki, Yumi
Kadooka, Keishi
Zhang, Pingbo
Fujii, Hiroshi
Amano, Maho
Nishimura, Shin-Ichiro
Tashiro, Kosuke
Kuhara, Satoru
Katakura, Yoshinori
spellingShingle Udono, Miyako
Fujii, Kaoru
Harada, Gakuro
Tsuzuki, Yumi
Kadooka, Keishi
Zhang, Pingbo
Fujii, Hiroshi
Amano, Maho
Nishimura, Shin-Ichiro
Tashiro, Kosuke
Kuhara, Satoru
Katakura, Yoshinori
Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells
author_facet Udono, Miyako
Fujii, Kaoru
Harada, Gakuro
Tsuzuki, Yumi
Kadooka, Keishi
Zhang, Pingbo
Fujii, Hiroshi
Amano, Maho
Nishimura, Shin-Ichiro
Tashiro, Kosuke
Kuhara, Satoru
Katakura, Yoshinori
author_sort Udono, Miyako
title Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells
title_short Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells
title_full Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells
title_fullStr Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells
title_full_unstemmed Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells
title_sort impaired atp6v0a2 expression contributes to golgi dispersion and glycosylation changes in senescent cells
description Many genes and signaling pathways have been found to be involved in cellular senescence program. In the present study, we have identified 16 senescence-associated genes by differential proteomic analysis of the normal human diploid fibroblast cell line, TIG-1, and focused on ATP6V0A2. The aim of this study is to clarify the role of ATP6V0A2, the causal gene for ARCL2, a syndrome of abnormal glycosylation and impaired Golgi trafficking, in cellular senescence program. Here we showed that ATP6V0A2 is critical for cellular senescence; impaired expression of ATP6V0A2 disperses the Golgi structure and triggers senescence, suggesting that ATP6V0A2 mediates these processes. FITC-lectin staining and glycoblotting revealed significantly different glycosylation structures in presenescent (young) and senescent (old) TIG-1 cells; reducing ATP6V0A2 expression in young TIG-1 cells yielded structures similar to those in old TIG-1 cells. Our results suggest that senescence-associated impaired expression of ATP6V0A2 triggers changes in Golgi structure and glycosylation in old TIG-1 cells, which demonstrates a role of ATP6V0A2 in cellular senescence program.
publisher Nature Publishing Group
publishDate 2015
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4661525/
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