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Laminar shear stress up-regulates peroxiredoxins (PRX) in endothelial cells: PRX 1 as a mechanosensitive antioxidant

Title
Laminar shear stress up-regulates peroxiredoxins (PRX) in endothelial cells: PRX 1 as a mechanosensitive antioxidant
Authors
Mowbray A.L.Kang D.-H.Sue G.R.Sang W.K.Jo H.
Ewha Authors
이서구강상원강동훈
SCOPUS Author ID
이서구scopusscopus; 강상원scopus; 강동훈scopus
Issue Date
2008
Journal Title
Journal of Biological Chemistry
ISSN
0021-9258JCR Link
Citation
vol. 283, no. 3, pp. 1622 - 1627
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Shear stress plays a significant role in endothelial cell biology and atherosclerosis development. Previous work by our group has shown that fluid flow stimulates important functional changes in cells through protein expression regulation. Peroxiredoxins (PRX) are a family of antioxidant enzymes but have yet to be investigated in response to shear stress. Studies have shown that oscillatory shear stress (OS) increases reactive oxygen species (ROS) levels in endothelial cells, whereas laminar shear stress (LS) blocks this response. We hypothesized that PRX are responsible for the anti-oxidative effect of LS. To test this hypothesis, bovine aortic endothelial cells (BAEC) were subjected to LS (15 dyn/cm2), OS (±5 dyn/cm2, 1 Hz), or static conditions for 24 h. Using Western blot and immunofluorescence staining, all six isoforms of PRX were identified in BAEC. When compared with OS and static, exposure to chronic LS up-regulated PRX 1 levels intracellularly. LS also increased expression of PRX 5 relative to static controls, but not OS. PRX exhibited broad subcellular localization, with distribution in the cytoplasm, Golgi, mitochondria, and intermediate filaments. In addition, PRX 1 knock down, using specific small interference RNA, attenuated LS-dependent reactive oxygen species reduction in BAEC. However, PRX 5 depletion did not. Together, these results suggest that PRX 1 is a novel mechanosensitive antioxidant, playing an important role in shear-dependent regulation of endothelial biology and atherosclerosis. © 2008 by The American Society for Biochemistry and Molecular Biology, Inc.
DOI
10.1074/jbc.M707985200
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일반대학원 > 생명·약학부 > Journal papers
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