title: Cyclic strain induces redox changes in endothelial cells.
abstract: Our previous studies have shown that cyclic strain to endothelial cells (ECs) increases reactive oxygen species (ROS) that act as second messengers. The potential impact of these enhanced ROS levels on ECs was examined by studying the antioxidant activities and heme oxygenase-1 (HO-1) expression in strained ECs. Cyclic strain to ECs increased lipid peroxidation and augmented oxidation of low-density lipoproteins. ECs subjected to strain increased their superoxide dismutase activities. Concomitantly, glutathione peroxidase activities increased in 3 to 6 hr and returned to basal level 24 hr after continuous cyclic strain treatment. A decrease of glutathione (GSH) was accompanied with an increase of oxidized glutathione (GSSH) level in ECs 3 to 6 hr after strain treatment. This was followed with a return of both GSH and GSSH to basal levels in 24 hr. Consistently, H2O2 treatment of ECs decreased the GSH/GSSG ratio. ECs pretreated with catalase abolished the strain-induced change in GSH/GSSG. Strain treatment, similar to H2O2 exposure, induced HO-1 expression in a time-dependent manner. This induction was inhibited after treating ECs with catalase or free radical scavenger. ECs treated with N-acetyl-cysteine abolished HO-1 gene induction. Our results suggest that cyclic strain-induced ROS cause a transient increase of glutathione peroxidase activity that results in a decrease of GSH level in ECs and that this decrease is crucial to HO-1 induction.
authors.affiliation: Cardiovascular Division, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.
authors.forename: J J
authors.initials: JJ
authors.lastname: Cheng
authors.forename: B S
authors.initials: BS
authors.lastname: Wung
authors.forename: Y J
authors.initials: YJ
authors.lastname: Chao
authors.forename: H J
authors.initials: HJ
authors.lastname: Hsieh
authors.forename: D L
authors.initials: DL
authors.lastname: Wang
mesh_terms: D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000201:enzymology / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000502:physiology; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000235:genetics; D051547:Heme Oxygenase-1; D006801:Humans; D007425:Intracellular Membranes / Q000378:metabolism; D008054:Lipid Peroxides / Q000096:biosynthesis; D008565:Membrane Proteins; D010084:Oxidation-Reduction; D010507:Periodicity; D017382:Reactive Oxygen Species / Q000378:metabolism; D013314:Stress, Mechanical; D013482:Superoxide Dismutase / Q000378:metabolism; D015533:Transcriptional Activation
chemical_list: D008054:Lipid Peroxides; D008565:Membrane Proteins; D017382:Reactive Oxygen Species; D005979:Glutathione Peroxidase; C496541:HMOX1 protein, human; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1; D013482:Superoxide Dismutase; D005978:Glutathione; D019803:Glutathione Disulfide