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Revealing the role of phosphatidylserine in shear stress-mediated protection in endothelial cells. Endothelium 2008 Jul-Aug;15(4):225-30 PMID: 18663626 PMCID: PMC2579788

Abstract

Previous studies have demonstrated that endothelial cells exposed to laminar shear stress are protected from apoptotic stimuli such as tumor necrosis factor (TNF)-alpha. The authors investigated the role of phosphatidylserine (PS) in this phenomenon. Western blot analysis of cleaved caspase 3 was used as an indicator of apoptosis and revealed that in the absence of serine, endothelial cells exposed to laminar shear stress were unable to protect against TNF-alpha-induced apoptosis, in contrast to sheared cells grown in regular medium. It was also found that shear-induced activation of the Akt pathway was significantly decreased in cells grown without serine. In addition, quantitation of PS using a novel isotopic labeling technique involving the use of formalin revealed that stearoyl-oleic PS (18:0/18:1) did not increase during shear treatment. These findings suggest that basal levels of PS are required to activate survival pathways in endothelial cells and thereby contribute to the overall protective mechanism initiated by shear stress.

Author List

Freed JK, Shortreed MR, Kleefisch CJ, Smith LM, Greene AS

Authors

Julie K. Freed MD, PhD Assistant Professor in the Anesthesiology department at Medical College of Wisconsin
Andrew S. Greene PhD Interim Vice Chair, Chief, Professor in the Biomedical Engineering department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Blood Flow Velocity
Endothelium, Vascular
Lipids
Mass Spectrometry
Phosphatidylserines
Rats
Rats, Sprague-Dawley
Stress, Mechanical
Tumor Necrosis Factor-alpha



View this publication's entry at the Pubmed website PMID: 18663626
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