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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2015
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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/ |
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Open Access Journal |
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Foreign Institution |
institution |
US National Center for Biotechnology Information |
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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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1613506739324321792 |