期刊
JOURNAL OF ENDOCRINOLOGY
卷 193, 期 1, 页码 137-145出版社
BIOSCIENTIFICA LTD
DOI: 10.1677/JOE-06-0173
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In this study, we investigated the in vivo role of adiponectin, an adipocytokine, on the development of atherosclerosis in rabbits mainly using adenovirus expressing adiponectin gene (Ad-APN) and intravascular ultrasonography. Serum adiponectin concentrations in rabbits after Ad-APN local transfer to abdominal aortas increased about nine times as much as those before transfer (P<0.01), about ten times as much as the levels of endogenous adiponectin in adenovirus expressing beta-galactosidase gene (Ad-beta gal) treated rabbits (P<0.01), and about four times as much as those in the aorta of non-injured rabbits on a normal cholesterol diet (P<0.01). Ultrasonography revealed a significantly reduced atherosclerotic plaque area in abdominal aortas of rabbits infected through intima with Ad-APN, by 35.2% compared with the area before treatment (P<0.01), and by 35.8% compared with that in Ad-beta gal-treated rabbits (P<0.01). In rabbits infected through adventitia, Ad-APN treatment reduced plaque area by 28.9% as compared with the area before treatment (P<0.01) and 25.6% compared with that in Ad-beta gal-treated rabbits (P<0.01). Adiponectin significantly suppressed the mRNA expression of vascular cell adhesion molecule-1 (VCAM-1) by 18.5% through intima transfer (P<0.05) and 26.9% through adventitia transfer (P<0.01), and intercellular adhesion molecule-1 (ICAM-1) by 40.7% through intima transfer (P<0.01), and 30.7% through adventitia transfer (P<0.01.). However, adiponectin had no effect on the expression of types I and III collagen. These results suggest that local adiponectin treatment suppresses the development of atherosclerosis in vivo in part by attenuating the expression of VCAM-1 and ICAM-1 in vascular walls.
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