Inflammation and enhanced atherogenesis in the carotid artery with altered blood flow in an atherosclerosis-resistant mouse strain.
Abstract
Ligation of the common carotid artery near its bifurcation in apolipoprotein E-deficient (Apoe-/- ) mice leads to rapid atherosclerosis development, which is affected by genetic backgrounds. BALB/cJ (BALB) mice are resistant to atherosclerosis, developing much smaller aortic lesions than C57BL/6 (B6) mice. In this study, we examined cellular events leading to lesion formation in carotid arteries with or without blood flow restriction of B6 and BALB Apoe-/- mice. Blood flow was obstructed by ligating the left common carotid artery near its bifurcation in one group of mice, and other group received no surgical intervention. Without blood flow interruption, BALB-Apoe-/- mice formed much smaller atherosclerotic lesions than B6-Apoe-/- mice after 12 weeks of Western diet (3,325 ± 1,086 vs. 81,549 ± 9,983 µm2 /section; p = 2.1E-7). Lesions occurred at arterial bifurcations in both strains. When blood flow was obstructed, ligated carotid artery of both strains showed notable lipid deposition, inflammatory cell infiltration, and rapid plaque formation. Neutrophils and macrophages were observed in the arterial wall of BALB mice 3 days after ligation and 1 week after ligation in B6 mice. CD4 T cells were observed in intimal lesions of BA...Continue Reading
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