Jian Zhao1,2, Chaoji Huangfu1,3, Zhihui Chang1,2, Andrew T Grainger4, Zhaoyu Liu2, Weibin Shi5,6. 1. Department of Radiology and Medical Imaging, University of Virginia, Charlottesville, Virginia, USA. 2. Department of Radiology, Shengjing Hospital of China Medical University, Shenyang, China. 3. Center for Disease Control and Prevention, Western Theater Command, Lanzhou, China. 4. Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia, USA. 5. Department of Radiology and Medical Imaging, University of Virginia, Charlottesville, Virginia, USA, ws4v@virginia.edu. 6. Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia, USA, ws4v@virginia.edu.
Abstract
PURPOSE: Atherosclerosis in the carotid arteries is a common cause of ischemic stroke. We examined atherogenesis in the left carotid artery with and without interrupted blood flow of C57BL/6 (B6) and C3H-Apoe-deficient (Apoe-/-) mouse strains. METHODS: Blood flow was interrupted by ligating the common carotid artery near its bifurcation in one group of mice and another group was not interrupted. RESULTS: Without interference with blood flow, C3H-Apoe-/- mice developed no atherosclerosis in the carotid artery, while B6-Apoe-/- mice formed advanced atherosclerotic lesions (98,019 ± 10,594 μm2/section) after 12 weeks of a Western diet. When blood flow was interrupted by ligating the common carotid artery near its bifurcation, C3H-Apoe-/- mice showed fatty streak lesions 2 weeks after ligation, and by 4 weeks fibrous lesions had formed, although they were smaller than in B6-Apoe-/- mice. Neutrophil adhesion to endothelium and infiltration in lesions was observed in ligated arteries of both strains. Treatment of B6-Apoe-/- mice with antibody against neutrophils had little effect on lesion size. CONCLUSIONS: These findings demonstrate the dramatic influences of genetic backgrounds and blood flow on atherogenesis in the carotid artery of hyperlipidemic mice.
PURPOSE:Atherosclerosis in the carotid arteries is a common cause of ischemic stroke. We examined atherogenesis in the left carotid artery with and without interrupted blood flow of C57BL/6 (B6) and C3H-Apoe-deficient (Apoe-/-) mouse strains. METHODS: Blood flow was interrupted by ligating the common carotid artery near its bifurcation in one group of mice and another group was not interrupted. RESULTS: Without interference with blood flow, C3H-Apoe-/- mice developed no atherosclerosis in the carotid artery, while B6-Apoe-/- mice formed advanced atherosclerotic lesions (98,019 ± 10,594 μm2/section) after 12 weeks of a Western diet. When blood flow was interrupted by ligating the common carotid artery near its bifurcation, C3H-Apoe-/- mice showed fatty streak lesions 2 weeks after ligation, and by 4 weeks fibrous lesions had formed, although they were smaller than in B6-Apoe-/- mice. Neutrophil adhesion to endothelium and infiltration in lesions was observed in ligated arteries of both strains. Treatment of B6-Apoe-/- mice with antibody against neutrophils had little effect on lesion size. CONCLUSIONS: These findings demonstrate the dramatic influences of genetic backgrounds and blood flow on atherogenesis in the carotid artery of hyperlipidemic mice.
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