title: Correlation of inflammatory cells in adventitia and formation and extending of atherosclerotic lesions in coronary artery of apolipoprotein E gene knockout mice.
abstract: Accumulating evidence shows that adventitial inflammation contributes to the development of atherosclerotic lesions. The aim of this study was to investigate the relationship between atherosclerotic lesions in coronary artery (CA) and accumulation of inflammatory cells at local adventitia in apolipoprotein E gene knockout (apoE-/-) mice. Modified Movat's pentachrome staining, HE staining, immunohistochemistry and transmission electron microscopy were used to observe and to identify serial paraffin sections of aortic foot and inflammatory cells in CA adventitia of apoE-/- mice of 60 weeks old. There was always accumulation of inflammatory cells in the adventitia of CA with extending lesions from aortic orifice to CA trunks. The CA samples were divided into type I: infiltration of inflammatory cells in CA adventitia without lesions extending in the intima, type II: infiltration of inflammatory cells in CA adventitia with the top of extending lesions in the intima and type III: infiltration of inflammatory cells at CA adventitia with lesions covering all the face of intima. The three types of CA sample represent the different developmental processes of atherosclerotic lesions, respectively. No extending lesions were found in the CA trunks without inflammatory cells in adventitia. In type I samples, 60% of infiltrated inflammatory cells were macrophages 57% of infiltrated cells were neutrophils in type II samples; 67% of infiltrated cells were lymphocytes in type III samples. Our studies revealed that adventitial inflammation may be an early event in the development of atherosclerotic lesions. Different cell types predominate in different stages of CA adventitia. The neutrophils are closely related to the extending of atherosclerotic lesions.
authors.affiliation: Department of Pathophysiology, School of Medicine, Shandong University, Jinan 250012, Shandong, PR China. wangmaq@sdu.edu.cn
authors.forename: Jian-Li
authors.initials: JL
authors.lastname: Wang
authors.forename: Si-Qin
authors.initials: SQ
authors.lastname: Ma
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Guo-Qing
authors.initials: GQ
authors.lastname: Liu
authors.forename: Wei-Cheng
authors.initials: WC
authors.lastname: Hu
authors.forename: Rong
authors.initials: R
authors.lastname: Ma
mesh_terms: D063194:Adventitia / Q000473:pathology*; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics / Q000502:physiology*; D018932:Chemokine CCL2 / Q000502:physiology; D003324:Coronary Artery Disease / Q000209:etiology* / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology*; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000473:pathology
chemical_list: D001057:Apolipoproteins E; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2