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

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

研究成果: Contribution to journalArticle査読

9 被引用数 (Scopus)

抄録

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, H2 can protect oxidation of this process.

本文言語英語
論文番号3606
ジャーナルScientific reports
7
1
DOI
出版ステータス出版済み - 12 1 2017

All Science Journal Classification (ASJC) codes

  • 一般

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