3.8 Article

Revealing the role of phosphatidylserine in shear stress-mediated protection in endothelial cells

Journal

ENDOTHELIUM-JOURNAL OF ENDOTHELIAL CELL RESEARCH
Volume 15, Issue 4, Pages 225-230

Publisher

INFORMA HEALTHCARE
DOI: 10.1080/10623320802228849

Keywords

endothelial cells; ESI-ToF; mass Spectrometry; TNF-alpha

Funding

  1. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL028182] Funding Source: NIH RePORTER
  2. NATIONAL HUMAN GENOME RESEARCH INSTITUTE [R01HG002298] Funding Source: NIH RePORTER
  3. NHGRI NIH HHS [R01-HG-02298] Funding Source: Medline
  4. NHLBI NIH HHS [N01-HV-28182, N01 HV028182] Funding Source: Medline

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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.

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