Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress

Abstract Based on the oxidative stress theory, aging derives from the accumulation of oxidized proteins induced by reactive oxygen species (ROS) in the cytoplasm. Hydrogen peroxide (H2O2) elicits ROS that induces skin aging through oxidation of proteins, forming disulfide bridges with cysteine or me...

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Autores principales:	Ching-Ying Wu, Wen-Li Hsu, Ming-Hsien Tsai, Jui-Lin Liang, Jian-He Lu, Chia-Jung Yen, Hsin-Su Yu, Mami Noda, Chi-Yu Lu, Chu-Huang Chen, Shian-Jang Yan, Tohru Yoshioka
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c4b49102e8a541c6904ff2fe0fb745b0
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spelling	oai:doaj.org-article:c4b49102e8a541c6904ff2fe0fb745b02021-12-02T16:08:19ZHydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress10.1038/s41598-017-03513-22045-2322https://doaj.org/article/c4b49102e8a541c6904ff2fe0fb745b02017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03513-2https://doaj.org/toc/2045-2322Abstract Based on the oxidative stress theory, aging derives from the accumulation of oxidized proteins induced by reactive oxygen species (ROS) in the cytoplasm. Hydrogen peroxide (H2O2) elicits ROS that induces skin aging through oxidation of proteins, forming disulfide bridges with cysteine or methionine sulfhydryl groups. Decreased Ca2+ signaling is observed in aged cells, probably secondary to the formation of disulfide bonds among Ca2+ signaling-related proteins. Skin aging processes are modeled by treating keratinocytes with H2O2. In the present study, H2O2 dose-dependently impaired the adenosine triphosphate (ATP)-induced Ca2+ response, which was partially protected via co-treatment with β-mercaptoethanol, resulting in reduced disulfide bond formation in inositol 1, 4, 5-trisphosphate receptors (IP3Rs). Molecular hydrogen (H2) was found to be more effectively protected H2O2-induced IP3R1 dysfunction by reducing disulfide bonds, rather than quenching ROS. In conclusion, skin aging processes may involve ROS-induced protein dysfunction due to disulfide bond formation, and H2 can protect oxidation of this process.Ching-Ying WuWen-Li HsuMing-Hsien TsaiJui-Lin LiangJian-He LuChia-Jung YenHsin-Su YuMami NodaChi-Yu LuChu-Huang ChenShian-Jang YanTohru YoshiokaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ching-Ying Wu Wen-Li Hsu Ming-Hsien Tsai Jui-Lin Liang Jian-He Lu Chia-Jung Yen Hsin-Su Yu Mami Noda Chi-Yu Lu Chu-Huang Chen Shian-Jang Yan Tohru Yoshioka Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress
description	Abstract Based on the oxidative stress theory, aging derives from the accumulation of oxidized proteins induced by reactive oxygen species (ROS) in the cytoplasm. Hydrogen peroxide (H2O2) elicits ROS that induces skin aging through oxidation of proteins, forming disulfide bridges with cysteine or methionine sulfhydryl groups. Decreased Ca2+ signaling is observed in aged cells, probably secondary to the formation of disulfide bonds among Ca2+ signaling-related proteins. Skin aging processes are modeled by treating keratinocytes with H2O2. In the present study, H2O2 dose-dependently impaired the adenosine triphosphate (ATP)-induced Ca2+ response, which was partially protected via co-treatment with β-mercaptoethanol, resulting in reduced disulfide bond formation in inositol 1, 4, 5-trisphosphate receptors (IP3Rs). Molecular hydrogen (H2) was found to be more effectively protected H2O2-induced IP3R1 dysfunction by reducing disulfide bonds, rather than quenching ROS. In conclusion, skin aging processes may involve ROS-induced protein dysfunction due to disulfide bond formation, and H2 can protect oxidation of this process.
format	article
author	Ching-Ying Wu Wen-Li Hsu Ming-Hsien Tsai Jui-Lin Liang Jian-He Lu Chia-Jung Yen Hsin-Su Yu Mami Noda Chi-Yu Lu Chu-Huang Chen Shian-Jang Yan Tohru Yoshioka
author_facet	Ching-Ying Wu Wen-Li Hsu Ming-Hsien Tsai Jui-Lin Liang Jian-He Lu Chia-Jung Yen Hsin-Su Yu Mami Noda Chi-Yu Lu Chu-Huang Chen Shian-Jang Yan Tohru Yoshioka
author_sort	Ching-Ying Wu
title	Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress
title_short	Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress
title_full	Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress
title_fullStr	Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress
title_full_unstemmed	Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress
title_sort	hydrogen gas protects ip3rs by reducing disulfide bridges in human keratinocytes under oxidative stress
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/c4b49102e8a541c6904ff2fe0fb745b0
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Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress

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