AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 295: H1966-H1973, 2008. First published September 12, 2008; doi:10.1152/ajpheart.00727.2008
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Laminar shear stress inhibits lipid peroxidation induced by high glucose plus arachidonic acid in endothelial cells

Gyeong In Mun,1 Sang Mi An,1 Heonyong Park,2 Hanjoong Jo,3 and Yong Chool Boo1

1Department of Molecular Medicine and Cell and Matrix Research Institute, BK21 Medical Education Program for Human Resources, Kyungpook National University School of Medicine, Daegu, Republic of Korea; 2Department of Molecular Biology and Institute of Nanosensor and Biotechnology, BK21 Graduate Program for RNA Biology, Dankook University, Seoul, Republic of Korea; and 3Wallace H. Coulter Department of Biomedical Engineering at Georgia Institute of Technology and Emory University, Atlanta, Georgia

Submitted 25 June 2008 ; accepted in final form 4 September 2008

Elevated blood glucose and free fatty acids induce oxidative stress associated with the incidence of cardiovascular disease. In contrast, laminar shear stress (LSS) plays a critical role in maintaining vascular health. The present study examined the mechanism for the antioxidant effect of LSS attenuating the oxidative stress induced by high glucose (HG) and arachidonic acid (AA) in human umbilical vein endothelial cells. HG and AA synergistically decreased cell viability and increased glutathione (GSH) oxidation and lipid peroxidation. The lipid peroxidation was markedly prevented by LSS as well as tetrahydrobiopterin (BH4) and GSH. LSS increased BH4 and GSH contents, and expression of GTP cyclohydrolase-1 and glutamylcysteine ligase (GCL) involved in their biosynthesis. Inhibition of GCL activity by DL-buthionine-(S,R)-sulfoximine and small-interfering RNA-mediated knockdown of GCL lessened the antioxidant effect of LSS. Therefore, it is suggested that LSS enhances antioxidant capacity of endothelial cells and thereby attenuates the oxidative stress caused by cardiovascular risk factors.

laminar shear stress; high glucose; arachidonic acid; lipid peroxidation; glutamylcysteine ligase


Address for reprint requests and other correspondence: Y. C. Boo, Dept. of Molecular Medicine, Kyungpook National Univ. School of Medicine, 101 dongin-dong 2-ga, Jung-gu, Daegu, 700-422, Republic of Korea (e-mail: ycboo{at}knu.ac.kr)






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