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  • 1
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; CELL ; Germany ; VITRO ; DISEASE ; MICE ; TIME ; MACROPHAGES ; SERA ; REDUCTION ; animals ; bone marrow ; BONE-MARROW ; DELETION ; NO ; LESIONS ; DIFFERENCE ; inactivation ; MUSCLE ; ATHEROSCLEROSIS ; DIET ; MOUSE MODEL ; VASCULATURE ; glucocorticoid receptor ; CALCIUM ; BEHAVIOR ; SMOOTH-MUSCLE ; inflammation ; SERUM ; PRODUCTS ; INCREASE ; DEFICIENT MICE ; GC ; methods ; dexamethasone ; USA ; BONE ; animal ; SMOOTH-MUSCLE-CELLS ; smooth muscle cells ; MEDIA ; RANKL ; VASCULAR CALCIFICATION ; MUSCLE-CELLS ; MARROW ; in vitro ; CRUCIAL ROLE ; DRIVEN ; ARTERIAL CALCIFICATION ; CHOLESTEROL-FED RABBITS ; CORONARY ANGIOPLASTY ; KAPPA-B LIGAND ; OSTEOPROTEGERIN ; RECEPTOR ACTIVATOR
    Abstract: Objective - Macrophage-derived products are known to play a crucial role during atherogenesis and vascular calcification. Glucocorticoids (GC) are important modulators of immune cell functions, but their specific effects on macrophages behavior during plaque formation are not defined. The present study was therefore designed to investigate the effects of macrophage-specific deletion of the glucocorticoid receptor (GR(LysMCre)) on atherogenesis and vascular calcification in a hyperlipidemic mouse-model. Methods and Results - Bone marrow was isolated from GRLysMCre mice and wild-type controls (GR(flox)) and subsequently transplanted into lethally irradiated LDL-receptor -deficient mice. Animals were fed a Western-type diet for 15 or 24 weeks, and atherosclerotic lesions within the aortic sinus were evaluated. At both time points, no significant difference in serum lipid and corticosterone concentrations, atherosclerotic lesion size and macrophage-content within the lesions could be observed. However, GRLysMCre mice showed less calcification as well as a significant reduction of RANKL, BMP2, and Msx2 expression within the vasculature. In vitro studies using conditioned media from macrophages which had been stimulated with dexamethasone demonstrated a dose-dependent increase in calcium deposition by vascular smooth muscle cells. Conclusion - This study demonstrates that macrophage-specific glucocorticoid receptor inactivation reduces vascular calcification without affecting atherosclerotic lesion size in LDL receptor -deficient mice. (Arterioscler Thromb Vasc Biol. 2008;28:2158-2164.)
    Type of Publication: Journal article published
    PubMed ID: 18787189
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  • 2
    ISSN: 1435-1285
    Keywords: Key words Atherosclerosis – inflammation – macrophages – smooth muscle cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Today, there is a wealth of information concerning the chronology of the cellular and molecular events associated with the development of cardiovascular diseases. It is now clear that atherosclerosis is largerly a result of a dysregulated fibroproliferative inflammatory response [1]. Treatment of cardiovascular disease is rapidly adapting to this new knowledge and the future holds great potential for preventing the disease by blocking the process at multiple stages. This short review provides an overview of the evolution of the atherosclerotic plaque. It focuses of three basic stages of the disease processes: initiation of the fatty streak, transition of the fatty streak to an atheroma, and progression and destabilization of the lesions leading to plaque rupture and occlusive thrombosis. It includes a discussion of the molecular and cellular biology of the atheraogenic process with an emphasis on key molecular mediators of the disease process and provides three tables which list examples of some of the key molecular mediators and the stages in which they are purported to play a role.
    Type of Medium: Electronic Resource
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