Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress
Year: 2017
Type: article
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.
Source: Scientific Reports
Institutions: Kaohsiung Medical University, Kaohsiung Medical University Chung-Ho Memorial Hospital, Kaohsiung Municipal Ta-Tung Hospital, National Cheng Kung University, Chi Mei Medical Center, National Health Research Institutes, Kyushu University, Texas Medical Center, New York Heart Research Foundation
Language: English
Subfield: Surgery
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,690
Awards: G2807317922, G3651991337, Role of Transient Receptor Potential Cation Channel, Subfamily C, Member 7 (Trpc7) in Response to Uvb Induced Skin Damage and Aging, Genetic model of hypothyroidism and analysis of pathological mechanism on neuropsychological symptoms, Role of Transient Receptor Potential (TRP) Channel in Response to UVB Induced Skin Damage and Aging
OpenAlex ID: W2622116029
