HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 283, Issue 3, 1622-1627, January 18, 2008

This Article Full Text Full Text (PDF) All Versions of this Article: 283/3/1622    most recent M707985200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mowbray, A. L. Articles by Jo, H. Search for Related Content PubMed PubMed Citation Articles by Mowbray, A. L. Articles by Jo, H. Social Bookmarking                      What's this?

Laminar Shear Stress Up-regulates Peroxiredoxins (PRX) in Endothelial Cells

PRX 1 AS A MECHANOSENSITIVE ANTIOXIDANT^*

Amy L. Mowbray, Dong-Hoon Kang, Sue Goo Rhee, Sang Won Kang^¶1, and Hanjoong Jo^||2

From the Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia 30322, Division of Life and Pharmaceutical Sciences and the Center for Cell Signaling and Drug Discovery Research, ^¶Department of Life Sciences, Ewha Womans University, Seoul 120-750, Korea, and ^||Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia 30322

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.

Received for publication, September 24, 2007 , and in revised form, October 23, 2007.

^* This work was supported by National Institutes of Health Grants HL71014, HL75209, and HL70531 (to H. J.) and 21C Frontier Functional Proteomics Project (FPR05C2-510) from the Korean Ministry of Science and Technology (to D. H. K. and S. W. K.) as well as an American Heart Association predoctoral fellowship (to A. L. M.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence may be addressed: Dept. of Life Sciences, 11-1 Daehyun-dong, Seodaemoon-gu, Seoul 120-750, Korea. Tel.: 82-2-3277-3352; Fax: 82-2-3277-3760; E-mail: kangsw{at}ewha.ac.kr.

² To whom correspondence may be addressed: Wallace H. Coulter Dept. of Biomedical Engineering at Georgia Tech and Emory University, 2005 WMB, Atlanta, GA 30322. Tel.: 404-712-9654; Fax: 404-727-3330; E-mail: hanjoong.jo{at}bme.gatech.edu.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				C. Hahn and M. A. Schwartz The Role of Cellular Adaptation to Mechanical Forces in Atherosclerosis Arterioscler. Thromb. Vasc. Biol., December 1, 2008; 28(12): 2101 - 2107. [Abstract] [Full Text] [PDF]

				G. I. Mun, S. M. An, H. Park, H. Jo, and Y. C. Boo Laminar shear stress inhibits lipid peroxidation induced by high glucose plus arachidonic acid in endothelial cells Am J Physiol Heart Circ Physiol, November 1, 2008; 295(5): H1966 - H1973. [Abstract] [Full Text] [PDF]

				J. Kisucka, A. K. Chauhan, I. S. Patten, A. Yesilaltay, C. Neumann, R. A. Van Etten, M. Krieger, and D. D. Wagner Peroxiredoxin1 Prevents Excessive Endothelial Activation and Early Atherosclerosis Circ. Res., September 12, 2008; 103(6): 598 - 605. [Abstract] [Full Text] [PDF]