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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.

Citation

Miyako Udono, Kaoru Fujii, Gakuro Harada, Yumi Tsuzuki, Keishi Kadooka, Pingbo Zhang, Hiroshi Fujii, Maho Amano, Shin-Ichiro Nishimura, Kosuke Tashiro, Satoru Kuhara, Yoshinori Katakura. Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells. Scientific reports. 2015;5:17342

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PMID: 26611489

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