Molecular mechanism of remodeling of autologous artery graft interposed to vein in rabbit.
Our previous study found that the artery interposed to vein did not develop atherosclerosis but rather underwent atrophic remodeling in hyperlipidemic rabbits, suggesting that local hemodynamic load was another important determinant for the development of atherosclerosis. This study focused on the cellular and molecular changes in autologous artery grafts derived from rabbits fed with high lipid diet for 1, 2, 4, 8, and 12 weeks. Thickness, area of vessel wall, and lumen area were measured and analyzed on the grafted common carotid artery (GCCA) interposed to vein and on the right common carotid artery. Apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling. Both elastin and collagen of GCCA were identified by the method of double stains of elastin and collagen. Reverse transcription polymerase chain reaction was used to observe matrix metalloproteinases (MMPs) mRNA expression changes in the examined arteries. The lumen area increased gradually in control common carotid artery and remained unchanged in GCCA 3 months later, since the surgery and the start of high lipid diet, while significantly increased apoptosis was evidenced from inner to outer part of GCCA. Collagen content decreased gradually and elastic fibers remained unchanged in GCCA. At 1 week after operation, the mRNA expression of MMP(2) and MMP(9) increased significantly and returned to baseline thereafter. The artery interposed to a vein underwent atrophy, characterized by increased apoptosis in the vessel wall from intima to adventitia, possibly due to low shear stress circumference and reduced vessel collagen resulting from postsurgical upregulated MMP(2) and MMP(9) expression.
Department of Pathology, Shanghai Public Health Clinical Center, Shanghai 201508, People's Republic of China.
Yanling
Y
Feng
Yanguo
Y
Shen
Hongqi
H
Zhang
D000818:Animals; D001158:Arteries / Q000473:pathology* / Q000503:physiopathology / Q000637:transplantation; D017536:Carotid Artery, Common / Q000378:metabolism / Q000503:physiopathology / Q000637:transplantation; D003324:Coronary Artery Disease / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D004195:Disease Models, Animal; D006083:Graft Occlusion, Vascular / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D006439:Hemodynamics / Q000502:physiology; D006949:Hyperlipidemias / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D011817:Rabbits; D013314:Stress, Mechanical; D014680:Veins / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery