SOXF: redox mediators of vascular smooth muscle cell growth

• Published in: British heart journal 2004-05, Vol.90 (5), p.488-490
• Main Authors: Jin, Z G, Berk, B C
• Format: Article
• Language: English
• Subjects: Ang II; angiotensin II; Animals; Apoptosis; atherosclerosis; Cardiovascular disease; Cell growth; cyclophilin A; Cyclophilin A - pharmacology; CyPA; Deoxyribonucleic acid; DNA; ERK; extracellular regulated signal kinase; Gene expression; Growth factors; heat shock protein 90; heat shock proteins; HSP90; HSP90 Heat-Shock Proteins - pharmacology; Humans; Kinases; Mini-Symposium; Mitogen-Activated Protein Kinase 1 - metabolism; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinases - metabolism; Muscle, Smooth, Vascular - growth & development; Oxidation-Reduction; Oxidative stress; Oxidative Stress - physiology; Pathogenesis; PDGF; peptidyl-prolyl cis-trans isomerase; Physiology; platelet derived growth factor; PPIase; Protein folding; Rats; reactive oxygen species; Reactive Oxygen Species - metabolism; Rodents; ROS; secreted oxidative stress induced factors; signal transduction; Smooth muscle; SOXF; Studies; Vascular Diseases - etiology; vascular smooth muscle; vascular smooth muscle cells; VSMC
• ISSN: 1355-6037; 0007-0769; 1468-201X
• DOI: 10.1136/hrt.2003.029371

Oxidative stress and the production of intracellular reactive oxygen species (ROS), such as superoxide (O2.-), hydrogen peroxide (H2O2), and hydroxyl radical (OH.), have been implicated in the pathogenesis of cardiovascular disease, in part by promoting vascular smooth muscle proliferation. 1- 4 Within the vessel wall, ROS are generated by several mechanisms, including vascular NAD(P)H oxidases. 5, 6 ROS formation can be stimulated by mechanical stress, environmental factors, platelet derived growth factor (PDGF), angiotensin II (Ang II), and low density lipoproteins. 7- 9 Because many risk factors for coronary artery disease such as hyperlipidaemia, hypertension, diabetes, and smoking increase production of ROS, it has been suggested that changes in vessel redox state are a common pathway involved in the pathogenesis of atherosclerosis and vascular injury. 1, 6, 10 Several key findings support the concept that ROS contribute to vascular diseases through effects on vascular smooth muscle cells (VSMC). CONCLUSION In summary, our recent studies demonstrate that CyPA and HSP90 are secreted redox sensitive mediators. Because both cyclophilins and heat shock proteins act as chaperones, their secretion suggests an important role in the stress response to ROS in maintaining normal protein folding and function.