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      Arterial Injury Increases Expression of Inflammatory Adhesion Molecules in the Carotid Arteries of Apolipoprotein-E-Deficient Mice<footref rid="foot01"> 1</footref>

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          Recent studies demonstrate increased cellular adhesion molecule expression by neointimal endothelium overlying primary and restenotic atherosclerotic plaque. In this study, we developed an atherosclerotic mouse model of arterial injury and characterized adhesion molecule expression after injury. Sixteen apolipoprotein-E-(ApoE)-deficient mice fed a Western-type diet for 4 weeks underwent carotid artery wire denudation at week 2. For each segment, the extent of neointima formation and medial thickening, or adhesion molecule expression, were scored separately on a scale from 0 (no plaque/thickening or expression) to 3 (extensive plaque/thickening or expression) using Movat staining (n = 3) or immunohistochemical analysis (n = 13). Histology revealed significant medial thickening (1.8 ± 0.9 vs. 0.3 ± 0.5, p < 0.001) versus controls and pronounced staining for monocytes/macrophages in the wall of injured vessels. Immunohistochemical analysis showed more robust expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on the luminal surface of injured arteries versus controls (2.2 ± 0.6 vs. 1.4 ± 0.7, p < 0.01, and 2.5 ± 0.5 vs. 1.2 ± 0.6, p < 0.001, respectively). Injury increased adventitial ICAM-1 expression (2.6 ± 0.5 vs. 1.6 ± 0.5, p < 0.002) and medial VCAM-1 expression (2.2 ± 0.6 vs. 1.2 ± 0.7, p < 0.004). Thus, carotid injury results in significant medial thickening and increases adhesion molecule expression beyond that induced in ApoE-deficient mice fed a Western diet alone. The observation of macrophage infiltration into the media at sites of increased ICAM-1 and VCAM-1 expression suggests that these molecules may mediate monocyte/macrophage trafficking into the wall of injured arteries.

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          Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages.

          Macrophage-derived foam cells express apolipoprotein E (apoE) abundantly in atherosclerotic lesions. To examine the physiologic role of apoE secretion by the macrophage in atherogenesis, bone marrow transplantation was used to reconstitute C57BL/6 mice with macrophages that were either null or wild type for the apoE gene. After 13 weeks on an atherogenic diet, C57BL/6 mice reconstituted with apoE null marrow developed 10-fold more atherosclerosis than controls in the absence of significant differences in serum cholesterol levels or lipoprotein profiles. ApoE expression was absent in the macrophage-derived foam cells of C57BL/6 mice reconstituted with apoE null marrow. Thus, lack of apoE expression by the macrophage promotes foam cell formation. These data support a protective role for apoE expression by the macrophage in early atherogenesis.
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            Cellular and molecular studies of atherogenesis.

             Russell Ross (1997)
            The lesions of atherosclerosis represent a protective, inflammatory-fibroproliferative response against the different agents which can cause the disease. With a chronic insult, the response may become excessive and thus constitute part of the disease process. The excessive response may be reversed, given sufficient opportunity for modification of the injurious factors. Approaches to modifying specific cellular interactions, growth-regulatory molecules or intracellular signaling molecules may afford opportunities for lesion prevention or regression. For further reading see [1,2].

              Author and article information

              J Vasc Res
              Journal of Vascular Research
              S. Karger AG
              October 1999
              28 October 1999
              : 36
              : 5
              : 372-378
              Departments of aBiomedical Engineering, bInternal Medicine and cCell Biology, University of Virginia, Health Sciences Centers, Charlottesville, Va., USA
              25676 J Vasc Res 1999;36:372–378
              © 1999 S. Karger AG, Basel

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              Figures: 5, References: 30, Pages: 7
              Research Paper


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