J. Lipid Res.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


A more recent version of this article appeared on April 1, 2006

Papers In Press, published online ahead of print January 17, 2006
J. Lipid Res., doi:10.1194/jlr.M500439-JLR200
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow Supplemental Data
Right arrow All Versions of this Article:
M500439-JLR200v1
47/4/715    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Byfield, F. J.
Right arrow Articles by Levitan, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Byfield, F. J.
Right arrow Articles by Levitan, I.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Submitted on October 5, 2005
Revised on December 27, 2005
Accepted on January 17, 2006

OxLDL increases endothelial stiffness, force generation and network formation

Fitzroy J. Byfield, Saloni Tikku, George H. Rothblat, Keith J. Gooch, and Irena Levitan

Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA 19104

Corresponding Author: fbyfield{at}mail.med.upenn.edu

This study investigates the effect of oxidatively modified low density lipoprotein (oxLDL) on the biomechanical properties of human aortic endothelial cells (HAECs). We show that treatment with oxLDL results in a 90% decrease in membrane deformability of HAECs as determined by micropipette aspiration. Furthermore, aortic endothelial cells freshly isolated from hypercholesterolemic pigs (PAECs) were significantly stiffer than cells isolated from healthy animals. Interestingly, oxLDL had no effect on membrane cholesterol of HAECs, but caused disappearance of a lipid raft marker, GM1, from the plasma membrane. Both, an increase in membrane stiffness and a disappearance of GM1 were also observed in cells that were cholesterol depleted by methyl-beta -cyclodextrin (Mbeta CD). Additionally, oxLDL treatment of HAECs embedded within collagen gels resulted in increased gel contraction, indicating an increase in force generation by the cells. This increase in force generation correlated with an increased ability of HAECs to elongate and form networks in a 3D environment. Increased force generation, elongation and network formation was also observed in cholesterol depleted cells. We suggest, therefore, that exposure to oxLDL results in disruption or redistribution of lipid rafts, which in turn induces stiffening of the endothelium, an increase in endothelial force generation and potential for network formation.


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


This article has been cited by other articles:


Home page
Am. J. Physiol. Cell Physiol.Home page
G. B. Kowalsky, F. J. Byfield, and I. Levitan
oxLDL facilitates flow-induced realignment of aortic endothelial cells
Am J Physiol Cell Physiol, August 1, 2008; 295(2): C332 - C340.
[Abstract] [Full Text] [PDF]


Home page
J. Cell Sci.Home page
M. Sun, N. Northup, F. Marga, T. Huber, F. J. Byfield, I. Levitan, and G. Forgacs
The effect of cellular cholesterol on membrane-cytoskeleton adhesion
J. Cell Sci., July 1, 2007; 120(13): 2223 - 2231.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Journal of Biological Chemistry 
 Molecular and Cellular Proteomics   ASBMB Today 
Copyright © 2006 by the American Society for Biochemistry and Molecular Biology.