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Background —A cytokine network is involved in atherogenesis. This study was conducted to investigate the effects of granulocyte-macrophage colony–stimulating factor (GM-CSF) on the development and composition of atherosclerotic lesions in Watanabe heritable hyperlipidemic (WHHL) rabbits.Methods and Results —GM-CSF (10 μg · kg−1 · d−1 ) was administered to 4-month-old WHHL rabbits (n=9) 5 days a week for 7.5 months, whereas an equal dose of human serum albumin was administered to controls (n=9). The cholesterol levels were not changed significantly by the treatment. Age-matched 4-month-old rabbits (n=7) had atheromatous plaques over 30.7±5.7% of the inner surface area of the aortic arch. After treatment, the percentages of surface atheromatous plaques to total aortic arch area were 45.0±12.6% in the GM-CSF group and 74.3±11.0% in controls (P &lt;0.0001). Histological examination demonstrated that GM-CSF reduced the ratio of intima to media (P &lt;0.01) and cross-sectional areas of atherosclerotic lesions (P &lt;0.0001). Quantitative analysis indicated a marked decrease in the areas of smooth muscle cells (P =0.0001), collagen (P =0.0001), and extracellular lipid deposits (P &lt;0.05) of atheromatous plaques in GM-CSF–treated rabbits compared with controls. The terminal deoxynucleotidyltransferase–mediated dUTP-digoxigenin nick end-labeling (TUNEL) method and immunohistochemistry were performed to examine the relationship between decreased atherosclerotic lesions and apoptosis. The percentage of TUNEL-positive cells increased in the GM-CSF group (GM-CSF, 24.1±4.4% versus control, 11.6±3.2%;P &lt;0.0001). GM-CSF enhanced the apoptosis of smooth muscle cells in the shoulder region and the fibrous cap (P &lt;0.0001), suggesting one of the mechanisms for the antiatherogenic effect.Conclusions —GM-CSF altered the composition of atherosclerotic lesions and reduced the atherosclerosis in WHHL rabbits.

circulation

Granulocyte-Macrophage Colony–Stimulating Factor Prevents the Progression of Atherosclerosis via Changes in the Cellular and Extracellular Composition of Atherosclerotic Lesions in Watanabe Heritable Hyperlipidemic Rabbits