title: Protective effect and mechanism of glutaredoxin 1 on coronary arteries endothelial cells damage induced by high glucose.
abstract: In recent years, diabetes and its associated complications have become a major public health concern. The cardiovascular risk increases significantly in diabetes patients. It is a complex disease characterized by multiple metabolic derangements and is known to impair cardiac function by disrupting the balance between pro-oxidants and antioxidants at the cellular level. The subsequent generation of reactive oxygen species (ROS) and accompanying oxidative stress are hallmarks of the molecular mechanisms responsible for cardiovascular disease. Protein thiols act as redox-sensitive switches and are believed to be a key element in maintaining the cellular redox balance. The redox state of protein thiols is regulated by oxidative stress and redox signaling and is important to cellular functions. The potential of the thiol-disulfide oxidoreductase enzymes (thioredoxin and glutaredoxin systems) in defense against oxidative stress has been noted previously. Increasing evidence demonstrates that glutaredoxin 1 (Grx1), a cytosolic enzyme responsible for the catalysis of protein deglutathionylation, plays distinct roles in inflammation and apoptosis by inducing changes in the cellular redox system. This study investigates whether and how Grx1 protects coronary artery vascular endothelial cells against high glucose (HG) induced damage. Results indicate that the activation of eNOS/NO system is regulated by Grx 1 and coupled with inhibition of JNK and NF-κB signaling pathway which could alleviate the oxidative stress and apoptosis damage in coronary arteries endothelial cells induced by HG.
authors.affiliation: Department of Biochemistry, Qiqihar Medical University, Qiqihar 161006, China.
authors.forename: Shuyan
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Clinical Pathogenic Microorganism, Qiqihar Medical University, Qiqihar 161006, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Sun
authors.affiliation: Department of Clinical Biochemistry, Qiqihar Medical University, Qiqihar 161006, China.
authors.forename: Xiaodan
authors.initials: X
authors.lastname: Qi
authors.affiliation: Department of Biochemistry, Qiqihar Medical University, Qiqihar 161006, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Shi
authors.affiliation: Department of Biochemistry, Qiqihar Medical University, Qiqihar 161006, China.
authors.forename: Han
authors.initials: H
authors.lastname: Gao
authors.affiliation: Department of Clinical Biochemistry, Qiqihar Medical University, Qiqihar 161006, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Wu
authors.affiliation: Department of Biochemistry, Qiqihar Medical University, Qiqihar 161006, China.
authors.forename: Xiucai
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Biology Genetics, Qiqihar Medical University, Qiqihar 161006, China.
authors.forename: Haitao
authors.initials: H
authors.lastname: Yu
authors.affiliation: Department of Biochemistry, Qiqihar Medical University, Qiqihar 161006, China.
authors.forename: Chunjing
authors.initials: C
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002478:Cells, Cultured; D003331:Coronary Vessels / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D019610:Cytoprotection; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D005947:Glucose / Q000008:administration & dosage*; D054477:Glutaredoxins / Q000008:administration & dosage*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013552:Swine
chemical_list: D054477:Glutaredoxins; D017382:Reactive Oxygen Species; D005947:Glucose
keywords: Grx 1; diabetes cardiovascular complications; eNOS/NO system; redox homeostasis; redox signaling pathway