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Blood, 1 December 2005, Vol. 106, No. 12, pp. 3691-3698.
Prepublished online as a Blood First Edition Paper on August 16, 2005; DOI 10.1182/blood-2005-06-2326.
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PLENARY PAPERS
Shear stress affects the intracellular distribution of eNOS: direct demonstration by a novel in vivo technique
Caroline Cheng,
Rien van Haperen,
Monique de Waard,
Luc C. A. van Damme,
Dennie Tempel,
Laurens Hanemaaijer,
Gert W. A. van Cappellen,
Joop Bos,
Cornelis J. Slager,
Dirk J. Duncker,
Anton F. W. van der Steen,
Rini de Crom, and
Rob Krams
From the Departments of Cardiology, Thoraxcenter, Cell Biology and Genetics, Development and Reproduction, Experimental Medical Instrumentation, and Vascular Surgery, Erasmus University Medical Center, Rotterdam, The Netherlands.
The focal location of atherosclerosis in the vascular tree is correlated with local variations in shear stress. We developed a method to induce defined variations in shear stress in a straight vessel segment of a mouse. To this end, a cylinder with a tapered lumen was placed around the carotid artery, inducing a high shear stress field. Concomitantly, regions of low shear stress and oscillatory shear stress were created upstream and down-stream of the device, respectively. This device was used in mice transgenic for an eNOS3GFP fusion gene. We observed a strong induction of endothelial nitric oxide synthase–green fluorescent protein (eNOS-GFP) mRNA expression in the high shear stress region compared with the other regions (P < .05). Quantification of eNOS-GFP fluorescence or of immunoreactivity to the Golgi complex or to platelet endothelial cell adhesion molecule 1 (PECAM-1) showed an increase in the high shear stress region (P < .05) compared with nontreated carotid arteries. Colocalization of eNOS-GFP with either the Golgi complex or PECAM-1 also responded to alterations of shear stress. In conclusion, we showed a direct response of mRNA and protein expression in vivo to induced variations of shear stress. This model provides the opportunity to study the relationship between shear stress alterations, gene expression, and atherosclerosis.
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