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ATP supplementation suppresses UVB‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2

BACKGROUND: Skin photoaging is the damage caused by excessive exposure to ultraviolet (UV) irradiation. We investigated the effect of adenosine triphosphate (ATP) supplementation on UVB‐induced photoaging in HaCaT cells and its potential molecular mechanism. MATERIALS AND METHODS: The toxicity of AT...

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Autores principales: Gan, Chunxia, Liu, Titi, Jia, Xiaorong, Huang, Xueqin, Qin, Xiangdong, Wang, Xuanjun, Sheng, Jun, Xu, Huanhuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10155794/
https://www.ncbi.nlm.nih.gov/pubmed/36973992
http://dx.doi.org/10.1111/srt.13303
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author Gan, Chunxia
Liu, Titi
Jia, Xiaorong
Huang, Xueqin
Qin, Xiangdong
Wang, Xuanjun
Sheng, Jun
Xu, Huanhuan
author_facet Gan, Chunxia
Liu, Titi
Jia, Xiaorong
Huang, Xueqin
Qin, Xiangdong
Wang, Xuanjun
Sheng, Jun
Xu, Huanhuan
author_sort Gan, Chunxia
collection PubMed
description BACKGROUND: Skin photoaging is the damage caused by excessive exposure to ultraviolet (UV) irradiation. We investigated the effect of adenosine triphosphate (ATP) supplementation on UVB‐induced photoaging in HaCaT cells and its potential molecular mechanism. MATERIALS AND METHODS: The toxicity of ATP on HaCaT cells was examined by the MTT assay. The effects of ATP supplementation on the viability and apoptosis of HaCaT cells were determined by crystal‐violet staining and flow cytometry, respectively. Cellular and mitochondrial ROS were stained using fluorescent dyes. Expression of Bax, B‐cell lymphoma (Bcl)‐2, sirtuin (SIRT)3, and superoxide dismutase (SOD)2 was measured via western blotting. RESULTS: ATP (1, 2 mM) exerted no toxic effect on the normal growth of HaCaT cells. UVB irradiation caused the apoptosis of HaCaT cells, and ATP supplementation inhibited the apoptosis induced by UVB significantly, as verified by expression of Bax and Bcl‐2. UVB exposure resulted in accumulation of cellular and mitochondrial reactive oxygen species (ROS), but ATP supplementation suppressed these increases. Expression of SIRT3 and SOD2 was decreased upon exposure to UVB irradiation but, under ATP supplementation, expression of SIRT3 and SOD2 was reversed, which was consistent with the reduction in ROS level observed in ATP‐treated HaCaT cells after exposure to UVB irradiation. CONCLUSIONS: ATP supplementation can suppress UVB irradiation‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2.
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spelling pubmed-101557942023-08-11 ATP supplementation suppresses UVB‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2 Gan, Chunxia Liu, Titi Jia, Xiaorong Huang, Xueqin Qin, Xiangdong Wang, Xuanjun Sheng, Jun Xu, Huanhuan Skin Res Technol Original Articles BACKGROUND: Skin photoaging is the damage caused by excessive exposure to ultraviolet (UV) irradiation. We investigated the effect of adenosine triphosphate (ATP) supplementation on UVB‐induced photoaging in HaCaT cells and its potential molecular mechanism. MATERIALS AND METHODS: The toxicity of ATP on HaCaT cells was examined by the MTT assay. The effects of ATP supplementation on the viability and apoptosis of HaCaT cells were determined by crystal‐violet staining and flow cytometry, respectively. Cellular and mitochondrial ROS were stained using fluorescent dyes. Expression of Bax, B‐cell lymphoma (Bcl)‐2, sirtuin (SIRT)3, and superoxide dismutase (SOD)2 was measured via western blotting. RESULTS: ATP (1, 2 mM) exerted no toxic effect on the normal growth of HaCaT cells. UVB irradiation caused the apoptosis of HaCaT cells, and ATP supplementation inhibited the apoptosis induced by UVB significantly, as verified by expression of Bax and Bcl‐2. UVB exposure resulted in accumulation of cellular and mitochondrial reactive oxygen species (ROS), but ATP supplementation suppressed these increases. Expression of SIRT3 and SOD2 was decreased upon exposure to UVB irradiation but, under ATP supplementation, expression of SIRT3 and SOD2 was reversed, which was consistent with the reduction in ROS level observed in ATP‐treated HaCaT cells after exposure to UVB irradiation. CONCLUSIONS: ATP supplementation can suppress UVB irradiation‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2. John Wiley and Sons Inc. 2023-03-13 /pmc/articles/PMC10155794/ /pubmed/36973992 http://dx.doi.org/10.1111/srt.13303 Text en © 2023 The Authors. Skin Research and Technology published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Gan, Chunxia
Liu, Titi
Jia, Xiaorong
Huang, Xueqin
Qin, Xiangdong
Wang, Xuanjun
Sheng, Jun
Xu, Huanhuan
ATP supplementation suppresses UVB‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2
title ATP supplementation suppresses UVB‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2
title_full ATP supplementation suppresses UVB‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2
title_fullStr ATP supplementation suppresses UVB‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2
title_full_unstemmed ATP supplementation suppresses UVB‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2
title_short ATP supplementation suppresses UVB‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2
title_sort atp supplementation suppresses uvb‐induced photoaging in hacat cells via upregulation of expression of sirt3 and sod2
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10155794/
https://www.ncbi.nlm.nih.gov/pubmed/36973992
http://dx.doi.org/10.1111/srt.13303
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