*BHF Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College London, London, UK; and â Institute for Nutrition Research, University of Oslo, Oslo, Norway Regions of the arterial tree exposed to laminar ï¬ow, which exerts high shear stress, are protected from inï¬ammation, endothelial cell (EC) death and atherosclerosis. TNF activates NF- B transcription factors, which potentially exert dual functions by inducing both proinï¬ammatory and cytoprotective transcripts. We assessed whether laminar shear stress protects EC by modulating NF- B function. Human umbilical vein EC (HUVEC) were cultured under shear stress (12 dynes/cm2 for 16 h) using a parallel-plate ï¬ow chamber or were maintained in static conditions. Comparative real-time PCR revealed that preshearing significantly alters transcriptional responses to TNF by enhancing the expression of cytoprotective molecules (Bcl-2, MnSOD, GADD45 , A1) and suppressing proinï¬ammatory transcripts (E-selectin, VCAM-1, IL-8). We demonstrated using assays of nuclear localization, NF- B subunit phosphorylation, DNA-binding, and transcriptional activity that NF- B is activated by TNF in presheared HUVEC. Furthermore, a speciï¬c inhibitor revealed that NF- B is essential for the induction of cytoprotective transcripts in presheared EC. Finally, we observed that NF- B can be activated in vascular endothelium exposed to laminar shear stress
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Laminar shear stress acts as a switch to regulate divergent functions of NF-κB in endothelial cells
Jason Partridge , Harald Carlsen , Karine Enesa , Hera Chaudhury , Mustafa Zakkar , Le Luong , Anne Kinderlerer , Mike Johns , Rune Blomhoff , Justin C. Mason , Dorian O. Haskard , and Paul C. Evans
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, Volume 21 (13): 3553
Fed of American Socs for Experimental Biology – Nov 1, 2007
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