CD68、α-SMA在老年人冠状动脉粥样硬化病变中表达及其意义
|
摘要
目的探讨CD68、α-SMA在老年人冠状动脉粥样硬化(atherosclerosis, As)病变和弥漫性内膜增厚(diffuse intimal thickening, DIT)中的表达及其与冠状As病变类型、管腔狭窄之间的关系及意义。
方法选用53例尸检病例的312块冠状动脉组织标本。光镜下诊断DIT和冠状As病变及其类型,用免疫组化和Scion图像软件系统,检测和计算冠状As病变中CD68-阳性巨噬细胞,α-SMA阳.性面积%,冠状动脉管腔狭窄程度面积%、脂质坏死核心(necrotic core, NC)和钙化基质面积%。
结果①在老年人冠状As病变类型和DIT中,40%(124/312)为DIT,5%(16/312)为Ⅰ型,10%(31/312)为Ⅱ型,21%(66/312)为Ⅲ型,4%(14/312)为Ⅳ型,18%(55/312)为V型和2%(6/312)为Ⅵ型；②脂质NC面积%在高胆固醇组明显大于正常胆固醇组(P<0.05),而钙化基质面积%在早期病变(Ⅰ-Ⅲ型)和进展期病变(Ⅳ-Ⅵ型)之间有显著性差异(P<0.05)；③冠状As病变CD68-阳性巨噬细胞随着冠状As病变进展和管腔狭窄程度的加重而增多,分别呈正相关(r=0.351,r=0.197,P<0.01),CD68-阳性巨噬细胞数在早期和进展期病变之间有显著性差异(P<0.01),在冠状AsⅣ型病变中,CD68-阳性巨噬细胞主要分布在斑块的肩部区；④冠状As病变内膜α-SMA阳性面积%随着冠状As病变进展和管腔狭窄程度的加重而减少,分别呈负相关(r=-0.494,r=-0.362,P<0.01),并在早期和进展期病变之间有显著性差异(P<0.05)；⑤CD68-阳性巨噬细胞、α-SMA阳性面积%在病变类型、管腔狭窄程度之间以及正常胆固醇和高胆固醇组之间有显著性差异(P<0.05)。
结论老年人冠状As病变内膜CD68阳.性巨噬细胞数增多及α-SMA阳性面积%减少始终始发和加重老年人冠状As病变的进展,大量巨噬细胞在肩部区浸润和脂质NC的增大与冠状As病变进展、不稳定斑块破裂及并发症的发生有关,高胆固醇促进冠状As病变VSMC的凋亡和／或死亡,VSMC主要由中膜迁移入内膜并增殖引起适应性冠状动脉DIT。
Objective To study the expression and significance of CD68,α-SMA in coronary ahtherosclerotic lesion and diffuse intimal thickening(DIT) of the aged, and the correlation among the expression of CD68, a-SMA and the lesion types of coronary atherosclerosis, the degree of luminal stenosis.
Methods 312 of coronary artery tissue samples were selected in 53 cases of autopsy. Using light microscope with HE staining, the DIT, coronary atherosclerotic lesion and its types were diagnosed, and Using immunohistochemistry and the Scion image software systems, it was detected and counted in the coronary atherosclerotic lesion and DIT that CD68-positive macrophages, area percentage of lumen stenosis, lipid necrotic core(NC) and calcifying matrix.
Results①There were 40%(124/312) of the DIT,5%(16/312) of typeⅠ,10%(31/312) of typeⅡ,21%(66/312) of typeⅢ,4%(14/312) of typeⅣ,18%(55/312) of typeV and 2%(6/312) of type VI in the atherosclerotic lesion types and DIT;②Area percentage of lipid NC was significantly greater in the high cholesterol group than in the normal cholesterol group(P<0.05), and area percentage of calcifying matrix was significant difference between early lesions(typeⅠ-Ⅲ) and advanced lesions(typeⅣ-Ⅵ,P<0.05);③CD68-positive macrophages in coronary atherosclerotic lesions were increased with progress of coronary atherosclerotic lesions and aggravation of luminal stenosis with positive correlation(r=0.351, r=0.197, P<0.01), but percentage of a-SMA-positive area were decreased with negative correlation(r=-0.494, r=-0.362, P<0.01), respectively, and CD68-positive macrophages and% of a-SMA-positive area had significant differences among lesion types, and degree of luminal stenosis as well as between normal cholesterol and high cholesterol groups(P<0.05).
Conclusions Increased infiltration of CD68-positive macrophages and decreased percentage of a-SMA-positive area in coronary atherosclerotic lesions all along initiates and aggravates the coronary atherosclerotic lesions, and a large number of macrophages mainly infiltrated in the shoulder area and increased lipid NC of plaque are associated with progress of coronary atherosclerotic lesions, unstable plaque rupture, the occurrence of complications in coronary atherosclerosis, and hypercholesterolemia contributes to the apoptosis and/or necrosis of VSMC of coronary atherosclerotic lesions, and the VSMC mainly migrate into the intima from tunica media and proliferation to result in DIT of coronary artery.
方法选用53例尸检病例的312块冠状动脉组织标本。光镜下诊断DIT和冠状As病变及其类型,用免疫组化和Scion图像软件系统,检测和计算冠状As病变中CD68-阳性巨噬细胞,α-SMA阳.性面积%,冠状动脉管腔狭窄程度面积%、脂质坏死核心(necrotic core, NC)和钙化基质面积%。
结果①在老年人冠状As病变类型和DIT中,40%(124/312)为DIT,5%(16/312)为Ⅰ型,10%(31/312)为Ⅱ型,21%(66/312)为Ⅲ型,4%(14/312)为Ⅳ型,18%(55/312)为V型和2%(6/312)为Ⅵ型；②脂质NC面积%在高胆固醇组明显大于正常胆固醇组(P<0.05),而钙化基质面积%在早期病变(Ⅰ-Ⅲ型)和进展期病变(Ⅳ-Ⅵ型)之间有显著性差异(P<0.05)；③冠状As病变CD68-阳性巨噬细胞随着冠状As病变进展和管腔狭窄程度的加重而增多,分别呈正相关(r=0.351,r=0.197,P<0.01),CD68-阳性巨噬细胞数在早期和进展期病变之间有显著性差异(P<0.01),在冠状AsⅣ型病变中,CD68-阳性巨噬细胞主要分布在斑块的肩部区；④冠状As病变内膜α-SMA阳性面积%随着冠状As病变进展和管腔狭窄程度的加重而减少,分别呈负相关(r=-0.494,r=-0.362,P<0.01),并在早期和进展期病变之间有显著性差异(P<0.05)；⑤CD68-阳性巨噬细胞、α-SMA阳性面积%在病变类型、管腔狭窄程度之间以及正常胆固醇和高胆固醇组之间有显著性差异(P<0.05)。
结论老年人冠状As病变内膜CD68阳.性巨噬细胞数增多及α-SMA阳性面积%减少始终始发和加重老年人冠状As病变的进展,大量巨噬细胞在肩部区浸润和脂质NC的增大与冠状As病变进展、不稳定斑块破裂及并发症的发生有关,高胆固醇促进冠状As病变VSMC的凋亡和／或死亡,VSMC主要由中膜迁移入内膜并增殖引起适应性冠状动脉DIT。
Objective To study the expression and significance of CD68,α-SMA in coronary ahtherosclerotic lesion and diffuse intimal thickening(DIT) of the aged, and the correlation among the expression of CD68, a-SMA and the lesion types of coronary atherosclerosis, the degree of luminal stenosis.
Methods 312 of coronary artery tissue samples were selected in 53 cases of autopsy. Using light microscope with HE staining, the DIT, coronary atherosclerotic lesion and its types were diagnosed, and Using immunohistochemistry and the Scion image software systems, it was detected and counted in the coronary atherosclerotic lesion and DIT that CD68-positive macrophages, area percentage of lumen stenosis, lipid necrotic core(NC) and calcifying matrix.
Results①There were 40%(124/312) of the DIT,5%(16/312) of typeⅠ,10%(31/312) of typeⅡ,21%(66/312) of typeⅢ,4%(14/312) of typeⅣ,18%(55/312) of typeV and 2%(6/312) of type VI in the atherosclerotic lesion types and DIT;②Area percentage of lipid NC was significantly greater in the high cholesterol group than in the normal cholesterol group(P<0.05), and area percentage of calcifying matrix was significant difference between early lesions(typeⅠ-Ⅲ) and advanced lesions(typeⅣ-Ⅵ,P<0.05);③CD68-positive macrophages in coronary atherosclerotic lesions were increased with progress of coronary atherosclerotic lesions and aggravation of luminal stenosis with positive correlation(r=0.351, r=0.197, P<0.01), but percentage of a-SMA-positive area were decreased with negative correlation(r=-0.494, r=-0.362, P<0.01), respectively, and CD68-positive macrophages and% of a-SMA-positive area had significant differences among lesion types, and degree of luminal stenosis as well as between normal cholesterol and high cholesterol groups(P<0.05).
Conclusions Increased infiltration of CD68-positive macrophages and decreased percentage of a-SMA-positive area in coronary atherosclerotic lesions all along initiates and aggravates the coronary atherosclerotic lesions, and a large number of macrophages mainly infiltrated in the shoulder area and increased lipid NC of plaque are associated with progress of coronary atherosclerotic lesions, unstable plaque rupture, the occurrence of complications in coronary atherosclerosis, and hypercholesterolemia contributes to the apoptosis and/or necrosis of VSMC of coronary atherosclerotic lesions, and the VSMC mainly migrate into the intima from tunica media and proliferation to result in DIT of coronary artery.
引文
[1]Ross R. The pathogenesis of atherosclerosis:a perspective for the 1990s[J]. Nature, 1993,362:801-809.
[2]Hansson GK, Jonasson L, Seifert PS, et al. Immune mechanisms in atherosclerosis[J]. Arteriosclerosis,1989,9:567-578.
[3]Indolfi C, Lorenzo ED, Perrino C, et al. Hydroxymethylglutaryl coenzyme A reductase inhibitor simvastatin prevents cardiac hypertrophy induced by pressure onverload and inhibits p21 ras activation [J]. Circulation,2002,106(16):2118-2124.
[4]Stary HC, Chandler AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis:A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association [J]. Arterioscler Thromb Vase Biol.1995,15:1512-1531.
[5]Sumiyoshi S, Nakashima Y, Chen Y-X, et al. Interleukin-10 expression is positively correlated with oxidized LDL deposition and inversely with T-lymphocyte infiltration in atherosclerotic intimas of human coronary arteries [J]. Pathol Res Pract,2006,202:141-50.
[6]Libby P, Aikawa M. Evolution and stabilization of vulnerable atherosclerotic plaque[J]. Jpn Circ J,2001,65:473-479
[7]Viles-Gonzalez JF, Fuster V, Badimon JJ. Links between inflammation and thrombogenicity in atherosclerosis[J]. Curr Mol Med,2006,6(5):489-499.
[8]Hansson GK, Libby P, Schonbeck U and Yan ZQ. Innate and adaptive immunity in the pathogenesis of atherosclerosis [J]. Circ Res,2002,91(4):281-291.
[9]Shiomi M, Fan J. Unstable coronary plaques and cardiac events in myocardial infarction-prone Watanabe heritable hyperlipidemic rabbits:questions and quandaries [J]. Curr Opin Lipidol,2008,19(6):631-636.
[10]Boyle JJ. Macrophage activation in atherosclerosis:Pathologenesis and pharmacology of plaque rupture[J]. Curr Vase Pharmacol,2005,3(1):63-74.
[11]Bradford.C. Berk. Vascular Smooth Muscle Growth:Autocrine Growth Mechanisms[J]. Physiol. Rev,2001,81:999-1030
[12]Friedrich C, Luft. Machanisms and cardiovascular damage in hypertension [J]. Hypertension,2001,37(Part 2):594-598.
[13]Moon SK, Thompson LJ, Madamanchi N, et al. Aging, oxidative responses, and proliferative capacity[J]. Am J Physiol Heart Circ Physiol,2001,280:2779-2788.
[14]Agrotis A, Kalinina N, Bobik A. Transforming growth factor-beta, cell signaling and cardiovascular disorders[J]. Curr Vase Pharmacol,2005,3:55-61.
[15]Bauriedel G, Hutter R, Welsch U, et al. Role of smooth muscle cell death in advanced coronary primary lesions:implications for plaque instability[J]. Cardiovasc Res,1999, 41(2):480-488.
[16]Nakashima Y, Chen YX, Kinukawa N, Sueishi K. Distributions of diffuse intimal thickening in human arteries:preferential expression in atherosclerosis-prone arteries from an early age[J]. Virchows Arch,2002,441:279-88.
[17]Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death. A comprehensive morphological classification scheme for atherosclerotic lesions[J]. Arterioscler Thromb Vase Biol,2000,20:1262-1275.
[18]Ruiz-Torres A, Gimeno A, Melon J, et al. Age-related loss of proliferative activity of human vascular smooth muscle cells in culture[J]. Mech Ageing Dev,1999,110:49-55.
[19]Bennett MR, Macdonald K, Chan SW, Boyle JJ, and Weissberg PL. Cooperative interactions between RB and p53 regulate cell proliferation, cell senescence, and apoptosis in human vascular smooth muscle cells from atherosclerotic plaques[J]. Circ Res.1998, 82:704-712.
[20]Ross R, Wight TN, Strandness E, and Thiele B. Human atherosclerosis I. Cell constitution and characteristics of advanced lesions of the superficial femoral artery [J]. Am J Pathol,1984,114:79-93.
[21]Ballinger SW, Patterson C, C-N Yan, et al. Hydrogen peroxide-and peroxynitrite-induced mitochondrial DNA damage and dysfunctionin vascular endothelial and smooth muscle cells[J]. Circ Res,2000,86:960-966.
[1]Lusis AJ. Atherosclerosis[J]. Nature,2000,407:233-241.
[2]Falk E. Pathogenesis of atherosclerosis[J]. J Am Coll Cardiol,2006,47:C7-C12.
[3]Geng YJ, Libby P. Progression of atheroma:a struggle between death and procreation[J]. Arterioscler Thromb Vasc Biol,2002,22:1370-1380.
[4]Gronholdt ML, Dalager-Pedersen S, Falk E. Coronary atherosclerosis:determinants of plaque rupture[J]. Eur Heart J,1998,19 SupplC:C24-C29.
[5]Newby AC, Zaltsman AB. Fibrous cap formation or destruction-the critical importance of vascular smooth muscle cell proliferation, migration and matrix formation[J]. Cardiovasc Res,1999,41:345-360.
[6]Owens GK, Kumar MS, Wamhoff BR. Molecular regulation of vascular smooth muscle cell differentiation in development and disease[J]. Physiol Rev,2004,84:767-801.
[7]Stary HC, Blankenhorn DH, Chandler AB, et al. A definition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association[J]. Arterioscler Thromb,1992,12:120-134.
[8]Stary HC, Chandler AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association[J]. Circulation.1995,92:1355-1374.
[9]Stary HC, Chandler AB, Glagov S, et al. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association[J]. Arterioscler Thromb. 1994,14:840-856.
[10]Herbert C. Stary, A. Bleakley Chandler, Robert E. Dinsmore, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis: a report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association[J]. Circulation,1995,92:1355-1374.
[11]Ross R. Atherosclerosis-an inflammatory disease. N Engl J Med,1999,340: 115-126.
[12]Navab M, Berliner JA, Watson AD, et al. The Yin and Yang of oxidation in the development of the fatty streak. A review based on the 1994 George Lyman Duff Memorial Lecture[J]. Arterioscler Thromb Vase Biol,1996,16:831-842.
[13]Steinberg Lewis AD. Conner Memorial Lecture. Oxidative modification of LDL and atherogenesis[J]. Circulation,1997,95:1062-1071.
[14]Eriksson EE, Xie X, Werr J, et al. Direct viewing of atherosclerosis in vivo:plaque invasion by leukocytes" is initiated by the endothelial selectins[J]. FASEB J,2001, 15:1149-1157.
[15]Nakashima Y, Raines EW, Plump AS, et al. Upregulation of VCAM-1 and ICAM-1 at atherosclerosis-prone sites on the endothelium in the ApoE-deficient mouse[J]. Arterioscler Thromb Vase Biol,1998,18:842-851.
[16]Schwartz CJ, Sprague EA, Kelley JL, et al. Aortic intimal monocyte recruitment in the norino and hypercholesterolemic baboon (Papio cynocephalus). An ultra-structural study: implications in atherogenesis[J]. Virchows Arch A Pathol Anat Histopathol,1985, 405:175-191.
[17]Jarrold BB, Bacon WL, and Velleman SG. Expression and localization of the proteoglycan decorin during the progression of cholesterol induced atherosclerosis in Japanese quail:implications for interaction with collagen type I and lipoproteins[J]. Atherosclerosis,1999,146:299-308.
[18]Stopeck AT, Nicholson AC, Mancini FP, et al. Cytokine regulation of low density lipoprotein receptor gene transcription in HepG2 cells[J]. J Biol Chem,1993, 268:17489-17494.
[19]Shi W, Haberland ME, Jien ML, Shih DM, and Lusis AJ. Endothelial responses to oxidized lipoproteins determine genetic susceptibility to atherosclerosis in mice[J]. Circulation,2000,102:75-81.
[20]Napoli C, D'Armiento FP, Mancini FP, et al. Fatty streak formation occurs in human fetal aortas and is greatly enhanced by maternal hypercholesterolemia. Intimal accumulation of low density lipoprotein and its oxidation precede monocyte recruitment into early atherosclerotic lesions[J]. J Clin Invest,1997,100:2680-2690.
[21]Abraham R, Choudhury A, Basu SK, et al. Disruption of T cell tolerance by directing a self antigen to macrophage-specific scavenger receptors[J]. J Immunol,1997, 158:4029-4035.
[22]Yla-Herttuala S, Palinski W, Butler SW, et al. Rabbit and human atherosclerotic lesions contain IgG that recognizes epitopes of oxidized LDL[J]. Arterioscler Thromb, 1994,14:32-40.
[23]Reckless J, Rubin EM, Verstuyft JB, et al. Monocyte chemoattractant protein-1 but not tumor necrosis factor-alpha is correlated with monocyte infiltration in mouse lipid lesions[J]. Circulation,1999,99:2310-2316.
[24]Zeindler CM, Kratky RG, and Roach MR. Quantitative measurements of early atherosclerotic lesions on rabbit aortae from vascular casts [J]. Atherosclerosis,1989, 76:245-255.
[25]Malinauskas RA, Herrmann RA, and Truskey GA. The distribution of intimal white blood cells in the normal rabbit aorta[J]. Atherosclerosis,1995,115:147-163.
[26]Atkinson JB, Harlan CW, Harlan GC, et al. The association of mast cells and atherosclerosis:a morphologic study of early atherosclerotic lesions in young people[J]. Hum Pathol,1994,25:154-159.
[27]Schwartz CJ, Sprague EA, Kelley JL, et al. Aortic intimal monocyte recruitment in the normo and hypercholesterolemic baboon(Papio cynocephalus). An ultra-structural study: implications in atherogenesis[J]. Virchows Arch A Pathol Anat Histopathol,1985, 405:175-191.
[28]Williams KJ and Tabas I. The response-to-retention hypothesis of early atherogenesis[J]. Arterioscler Thromb Vasc Biol,1995,15:551-561.
[29]McIntyre TM, Zimmerman GA, and Prescott SM. Leukotrienes C4 and D4 stimulate human endothelial cells to synthesize platelet-activating factor and bind neutrophils[J]. Proc Natl Acad Sci USA,1986,83:2204-2208.
[30]Nakashima Y, Raines EW, Plump AS, et al. Upregulation of VCAM-1 and ICAM-1 at atherosclerosis-prone sites on the endothelium in the ApoE-deficient mouse[J]. Arterioscler Thromb Vasc Biol,1998,18:842-851.
[31]Lessner SM, Prado HL, Waller EK, et al. Atherosclerotic lesions grow through recruitment and proliferation of circulating monocytes in a murine model [J]. Am J Pathol, 2002,160:2145-2155.
[32]Iiyama K, Hajra L, Iiyama M, et al. Patterns of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression in rabbit and mouse atherosclerotic lesions and at sites predisposed to lesion formation[J]. Circ Res,1999,85:199-207.
[33]Rosenfeld ME. Leukocyte recruitment into developing atherosclerotic lesions:the complex interaction between multiple molecules keeps getting more complex[J]. Arterioscler Thromb Vasc Biol,2003,22:361-363.
[34]Allen S, Khan S, Al-Mohanna F, Batten P, and Yacoub M. Native low density lipoprotein-induced calcium transients trigger VCAM-1 and E-selectin expression in cultured human vascular endothelial cells[J]. J Clin Invest,1998,101:1064-1075.
[35]Ley K. Molecular mechanisms of leukocyte recruitment in the inflammatory process[J]. Cardiovasc Res,1996,32:733-742.
[36]Weninger WJ, Muller GB, Reiter C, et al. Intimal hyperplasia of the infant parasellar carotid artery:a potential developmental factor in atherosclerosis and SIDS[J]. Circ Res, 1999,85:970-975.
[37]Stary HC. Natural history and histological classification of atherosclerotic lesions:an update[J]. Arterioscler Thromb Vasc Biol,2000,20:1177-1178.
[38]Ikari Y, McManus BM, Kenyon J, Schwartz SM. Neonatal intima formation in the human coronary artery [J]. Arterioscler Thromb Vasc Biol,1999,19:2036-2040.
[39]Schwartz SM, Murry CE. Proliferation and the monoclonal origins of atherosclerotic lesions[J]. Annu Rev Med,1998,49:437-460.
[40]Mosse PR, Campbell GR, Wang ZL, Campbell JH. Smooth muscle phenotypic expression in human carotid arteries. I. Comparison of cells from diffuse intimal thickenings adjacent to atheromatous plaques with those of the media[J]. Lab Invest,1985, 53:556-562.
[41]Worth NF, Rolfe BE, Song J, Campbell GR. Vascular smooth muscle cell phenotypic modulation in culture is associated with reorganisation of contractile and cytoskeletal proteins[J]. Cell Motil Cytoskeleton,2001,49:130-145.
[42]Thyberg J, Hultgardh-Nilsson A. Fibronectin and the basement membrane components laminin and collagen type IV influence the phenotypic properties of subcultured rat aortic smooth muscle cells differently[J]. Cell Tissue Res,1994, 276:263-271.
[43]Li X, Van Putten V, Zarinetchi F, et al. Suppression of smooth-muscle alpha-actin expression by platelet-derived growth factor in vascular smooth-muscle cells involves Ras and cytosolic phospholipase A2[J]. Biochem J,1997,327 (Pt 3):709-716.
[44]Reusch P, Wagdy H, Reusch R, et al. Mechanical strain increases smooth muscle and decreases nonmuscle myosin expression in rat vascular smooth muscle cells[J]. Circ Res, 1996,79:1046-1053.
[45]Su B, Mitra S, Gregg H, et al. Redox regulation of vascular smooth muscle cell differentiation[J]. Circ Res,2001,89:39-46.
[46]Pidkovka NA, Cherepanova OA, Yoshida T, et al. Oxidized phospholipids induce phenotypic switching of vascular smooth muscle cells in vivo and in vitro[J]. Circ Res, 2007,101:792-801.
[47]Ang AH, Tachas G, Campbell JH, et al. Collagen synthesis by cultured rabbit aortic smooth-muscle cells[J]. Alteration with phenotype. Biochem J,1990,265:461-469.
[48]Rong JX, Shapiro M, Trogan E, Fisher EA. Transdifferentiation of mouse aortic smooth muscle cells to a macrophage-like state after cholesterol loading[J]. Proc Natl Acad Sci U S A,2003,100:13531-13536.
[49]Ruan XZ, Moorhead JF, Tao JL, et al. Mechanisms of dysregulation of low-density lipoprotein receptor expression in vascular smooth muscle cells by inflammatory cytokines[J]. Arterioscler Thromb Vasc Biol,2006,26:1150-1155.
[50]Takahashi M, Takahashi S, Suzuki C, et al. IL-1 beta attenuates beta-very low-density lipoprotein uptake and its receptor expression in vascular smooth muscle cells[J]. J Mol Cell Cardiol,2005,38:637-646.
[51]Matsumoto K, Hirano K, Nozaki S, et al. Expression of macrophage (Mphi) scavenger receptor, CD36, in cultured human aortic smooth muscle cells in association with expression of peroxisome proliferator activated receptor-gamma, which regulates gain of Mphi-like phenotype in vitro, and its implication in atherogenesis[J]. Arterioscler Thromb Vasc Biol,2000,20:1027-1032.
[52]Wagsater D, Olofsson PS, Norgren L, et al. The chemokine and scavenger receptor CXCL16/SR-PSOX is expressed in human vascular smooth muscle cells and is induced by INF gamma[J]. Biochem Biophys Res Commun,2004,325:1187-1193.
[53]Botham KM, Bravo E, Elliott J, et al. Direct interaction of dietary lipids carried in chylomicron remnants with cells of the artery wall:implications for atherosclerosis development[J]. Curr Pharm Des,2005,11:3681-3695.
[54]Nagao S, Murao K, Imachi H, et al. Platelet derived growth factor regulates ABCA1 expression in vascular smooth muscle cells[J]. FEBS Lett,2006,580:4371-4376.
[55]Huo Y, Ley K. Adhesion molecules and atherogenesis[J]. Acta Physiol Scand,2001, 173:35-43.
[56]50. Braun M, Pietsch P, Schror K, et al. Cellular adhesion molecules on vascular smooth muscle cells[J]. Cardiovasc Res,1999,41:395-401.
[57]Cai Q, Lanting L, Natarajan R. Interaction of monocytes with vascular smooth muscle cells regulates monocyte survival and differentiation through distinct pathways[J]. Arterioscler Thromb Vasc Biol,2004,24:2263-2270.
[58]Jang Y, Lincoff AM, Plow ejectionfactor (EF), et al. Cell adhesion molecules in coronary artery disease[J]. J Am Coll Cardiol,1994,24:1591-1601.
[59]Endres M, Laufs U, Merz H, et al. Focal expression of intercellular adhesion molecule-1 in the human carotid bifurcation[J]. Stroke,1997,28:77-82.
[60]Wong BW, Wong D, McManus BM. Characterization of fractalkine (CX3CL1) and CX3CR1 in human coronary arteries with native atherosclerosis, diabetes mellitus, and transplant vascular disease[J]. Cardiovasc Pathol,2002,11:332-338.
[61]Barlic J, Zhang Y, Foley JF, et al. Oxidized lipid-driven chemokine receptor switch, CCR2 to CX3CR1, mediates adhesion of human macrophages to coronary artery smooth muscle cells through a peroxisome proliferator-activated receptor gamma-dependent pathway[J]. Circulation,2006,114:807-819.
[62]Barlic J, Zhang Y, Murphy PM. Atherogenic lipids induce adhesion of human coronary artery smooth muscle cells to macrophages by up-regulating chemokine CX3CL1 on smooth muscle cells in a TNFalpha-NF kappa B-dependent manner [J]. J Biol Chem, 2007,282:19167-19176.
[63]Isner JM, Kearney M, Bortman S, Passeri J. Apoptosis in human atherosclerosis and restenosis[J]. Circulation,1995,91:2703-2711.
[64]Raines EW, Ferri N. Thematic review series:The immune system and atherogenesis. Cytokines affecting endothelial and smooth muscle cells in vascular disease[J]. J Lipid Res, 2005,46:1081-1092.
[65]Engelberg H. Endogenous heparin activity deficiency:the'missing link'in atherogenesis? [J]. Atherosclerosis,2001,159:253-260.
[66]O'Brien KD, Olin KL, Alpers CE, et al. Comparison of apolipoprotein and proteoglycan deposits in human coronary atherosclerotic plaques:colocalization of biglycan with apolipoproteins[J]. Circulation,1998,98:519-527.
[67]Chait A, Wight TN. Interaction of native and modified low-density lipoproteins with extracellular matrix[J]. Curr Opin Lipidol,2000,11:457-463.
[68]Camejo G, Fager G, Rosengren B, Hurt-Camejo E, Bondjers G. Binding of low density lipoproteins by proteoglycans synthesized by proliferating and quiescent human arterial smooth muscle cells[J]. J Biol Chem,1993,268:14131-14137.
[69]Chang MY, Potter-Perigo S, Tsoi C, et al. Oxidized low density lipoproteins regulate synthesis of monkey aortic smooth muscle cell proteoglycans that have enhanced native low density lipoprotein binding properties [J]. J Biol Chem,2000,275:4766-4773.
[70]Bond M, Sala-Newby GB, Newby AC. Focal adhesion kinase (FAK)-dependent regulation of S-phase kinase-associated protein-2 (Skp-2) stability. A novel mechanism regulating smooth muscle cell proliferation[J]. J Biol Chem,2004,279:37304-37310.
[71]Koyama H, Raines EW, Bornfeldt KE, et al. Fibrillar collagen inhibits arterial smooth muscle proliferation through regulation of Cdk2 inhibitors[J]. Cell,1996,87:1069-1078.
[72]Roy J, Tran PK, Religa P, Kazi M, et al. Fibronectin promotes cell cycle entry in smooth muscle cells in primary culture[J]. Exp Cell Res,2002,273:169-177.
[73]Edwards IJ, Wagner WD. Distinct synthetic and structural characteristics of proteoglycans produced by cultured artery smooth muscle cells of atherosclerosis-susceptible pigeons[J]. J Biol Chem.1988;263: 9612-9620.
[74]Wight TN, Kinsella MG, Lark MW, et al. Vascular cell proteoglycans:evidence for metabolic modulation[J]. Ciba Found Symp,1986,124:241-259.
[2]Hansson GK, Jonasson L, Seifert PS, et al. Immune mechanisms in atherosclerosis[J]. Arteriosclerosis,1989,9:567-578.
[3]Indolfi C, Lorenzo ED, Perrino C, et al. Hydroxymethylglutaryl coenzyme A reductase inhibitor simvastatin prevents cardiac hypertrophy induced by pressure onverload and inhibits p21 ras activation [J]. Circulation,2002,106(16):2118-2124.
[4]Stary HC, Chandler AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis:A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association [J]. Arterioscler Thromb Vase Biol.1995,15:1512-1531.
[5]Sumiyoshi S, Nakashima Y, Chen Y-X, et al. Interleukin-10 expression is positively correlated with oxidized LDL deposition and inversely with T-lymphocyte infiltration in atherosclerotic intimas of human coronary arteries [J]. Pathol Res Pract,2006,202:141-50.
[6]Libby P, Aikawa M. Evolution and stabilization of vulnerable atherosclerotic plaque[J]. Jpn Circ J,2001,65:473-479
[7]Viles-Gonzalez JF, Fuster V, Badimon JJ. Links between inflammation and thrombogenicity in atherosclerosis[J]. Curr Mol Med,2006,6(5):489-499.
[8]Hansson GK, Libby P, Schonbeck U and Yan ZQ. Innate and adaptive immunity in the pathogenesis of atherosclerosis [J]. Circ Res,2002,91(4):281-291.
[9]Shiomi M, Fan J. Unstable coronary plaques and cardiac events in myocardial infarction-prone Watanabe heritable hyperlipidemic rabbits:questions and quandaries [J]. Curr Opin Lipidol,2008,19(6):631-636.
[10]Boyle JJ. Macrophage activation in atherosclerosis:Pathologenesis and pharmacology of plaque rupture[J]. Curr Vase Pharmacol,2005,3(1):63-74.
[11]Bradford.C. Berk. Vascular Smooth Muscle Growth:Autocrine Growth Mechanisms[J]. Physiol. Rev,2001,81:999-1030
[12]Friedrich C, Luft. Machanisms and cardiovascular damage in hypertension [J]. Hypertension,2001,37(Part 2):594-598.
[13]Moon SK, Thompson LJ, Madamanchi N, et al. Aging, oxidative responses, and proliferative capacity[J]. Am J Physiol Heart Circ Physiol,2001,280:2779-2788.
[14]Agrotis A, Kalinina N, Bobik A. Transforming growth factor-beta, cell signaling and cardiovascular disorders[J]. Curr Vase Pharmacol,2005,3:55-61.
[15]Bauriedel G, Hutter R, Welsch U, et al. Role of smooth muscle cell death in advanced coronary primary lesions:implications for plaque instability[J]. Cardiovasc Res,1999, 41(2):480-488.
[16]Nakashima Y, Chen YX, Kinukawa N, Sueishi K. Distributions of diffuse intimal thickening in human arteries:preferential expression in atherosclerosis-prone arteries from an early age[J]. Virchows Arch,2002,441:279-88.
[17]Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death. A comprehensive morphological classification scheme for atherosclerotic lesions[J]. Arterioscler Thromb Vase Biol,2000,20:1262-1275.
[18]Ruiz-Torres A, Gimeno A, Melon J, et al. Age-related loss of proliferative activity of human vascular smooth muscle cells in culture[J]. Mech Ageing Dev,1999,110:49-55.
[19]Bennett MR, Macdonald K, Chan SW, Boyle JJ, and Weissberg PL. Cooperative interactions between RB and p53 regulate cell proliferation, cell senescence, and apoptosis in human vascular smooth muscle cells from atherosclerotic plaques[J]. Circ Res.1998, 82:704-712.
[20]Ross R, Wight TN, Strandness E, and Thiele B. Human atherosclerosis I. Cell constitution and characteristics of advanced lesions of the superficial femoral artery [J]. Am J Pathol,1984,114:79-93.
[21]Ballinger SW, Patterson C, C-N Yan, et al. Hydrogen peroxide-and peroxynitrite-induced mitochondrial DNA damage and dysfunctionin vascular endothelial and smooth muscle cells[J]. Circ Res,2000,86:960-966.
[1]Lusis AJ. Atherosclerosis[J]. Nature,2000,407:233-241.
[2]Falk E. Pathogenesis of atherosclerosis[J]. J Am Coll Cardiol,2006,47:C7-C12.
[3]Geng YJ, Libby P. Progression of atheroma:a struggle between death and procreation[J]. Arterioscler Thromb Vasc Biol,2002,22:1370-1380.
[4]Gronholdt ML, Dalager-Pedersen S, Falk E. Coronary atherosclerosis:determinants of plaque rupture[J]. Eur Heart J,1998,19 SupplC:C24-C29.
[5]Newby AC, Zaltsman AB. Fibrous cap formation or destruction-the critical importance of vascular smooth muscle cell proliferation, migration and matrix formation[J]. Cardiovasc Res,1999,41:345-360.
[6]Owens GK, Kumar MS, Wamhoff BR. Molecular regulation of vascular smooth muscle cell differentiation in development and disease[J]. Physiol Rev,2004,84:767-801.
[7]Stary HC, Blankenhorn DH, Chandler AB, et al. A definition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association[J]. Arterioscler Thromb,1992,12:120-134.
[8]Stary HC, Chandler AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association[J]. Circulation.1995,92:1355-1374.
[9]Stary HC, Chandler AB, Glagov S, et al. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association[J]. Arterioscler Thromb. 1994,14:840-856.
[10]Herbert C. Stary, A. Bleakley Chandler, Robert E. Dinsmore, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis: a report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association[J]. Circulation,1995,92:1355-1374.
[11]Ross R. Atherosclerosis-an inflammatory disease. N Engl J Med,1999,340: 115-126.
[12]Navab M, Berliner JA, Watson AD, et al. The Yin and Yang of oxidation in the development of the fatty streak. A review based on the 1994 George Lyman Duff Memorial Lecture[J]. Arterioscler Thromb Vase Biol,1996,16:831-842.
[13]Steinberg Lewis AD. Conner Memorial Lecture. Oxidative modification of LDL and atherogenesis[J]. Circulation,1997,95:1062-1071.
[14]Eriksson EE, Xie X, Werr J, et al. Direct viewing of atherosclerosis in vivo:plaque invasion by leukocytes" is initiated by the endothelial selectins[J]. FASEB J,2001, 15:1149-1157.
[15]Nakashima Y, Raines EW, Plump AS, et al. Upregulation of VCAM-1 and ICAM-1 at atherosclerosis-prone sites on the endothelium in the ApoE-deficient mouse[J]. Arterioscler Thromb Vase Biol,1998,18:842-851.
[16]Schwartz CJ, Sprague EA, Kelley JL, et al. Aortic intimal monocyte recruitment in the norino and hypercholesterolemic baboon (Papio cynocephalus). An ultra-structural study: implications in atherogenesis[J]. Virchows Arch A Pathol Anat Histopathol,1985, 405:175-191.
[17]Jarrold BB, Bacon WL, and Velleman SG. Expression and localization of the proteoglycan decorin during the progression of cholesterol induced atherosclerosis in Japanese quail:implications for interaction with collagen type I and lipoproteins[J]. Atherosclerosis,1999,146:299-308.
[18]Stopeck AT, Nicholson AC, Mancini FP, et al. Cytokine regulation of low density lipoprotein receptor gene transcription in HepG2 cells[J]. J Biol Chem,1993, 268:17489-17494.
[19]Shi W, Haberland ME, Jien ML, Shih DM, and Lusis AJ. Endothelial responses to oxidized lipoproteins determine genetic susceptibility to atherosclerosis in mice[J]. Circulation,2000,102:75-81.
[20]Napoli C, D'Armiento FP, Mancini FP, et al. Fatty streak formation occurs in human fetal aortas and is greatly enhanced by maternal hypercholesterolemia. Intimal accumulation of low density lipoprotein and its oxidation precede monocyte recruitment into early atherosclerotic lesions[J]. J Clin Invest,1997,100:2680-2690.
[21]Abraham R, Choudhury A, Basu SK, et al. Disruption of T cell tolerance by directing a self antigen to macrophage-specific scavenger receptors[J]. J Immunol,1997, 158:4029-4035.
[22]Yla-Herttuala S, Palinski W, Butler SW, et al. Rabbit and human atherosclerotic lesions contain IgG that recognizes epitopes of oxidized LDL[J]. Arterioscler Thromb, 1994,14:32-40.
[23]Reckless J, Rubin EM, Verstuyft JB, et al. Monocyte chemoattractant protein-1 but not tumor necrosis factor-alpha is correlated with monocyte infiltration in mouse lipid lesions[J]. Circulation,1999,99:2310-2316.
[24]Zeindler CM, Kratky RG, and Roach MR. Quantitative measurements of early atherosclerotic lesions on rabbit aortae from vascular casts [J]. Atherosclerosis,1989, 76:245-255.
[25]Malinauskas RA, Herrmann RA, and Truskey GA. The distribution of intimal white blood cells in the normal rabbit aorta[J]. Atherosclerosis,1995,115:147-163.
[26]Atkinson JB, Harlan CW, Harlan GC, et al. The association of mast cells and atherosclerosis:a morphologic study of early atherosclerotic lesions in young people[J]. Hum Pathol,1994,25:154-159.
[27]Schwartz CJ, Sprague EA, Kelley JL, et al. Aortic intimal monocyte recruitment in the normo and hypercholesterolemic baboon(Papio cynocephalus). An ultra-structural study: implications in atherogenesis[J]. Virchows Arch A Pathol Anat Histopathol,1985, 405:175-191.
[28]Williams KJ and Tabas I. The response-to-retention hypothesis of early atherogenesis[J]. Arterioscler Thromb Vasc Biol,1995,15:551-561.
[29]McIntyre TM, Zimmerman GA, and Prescott SM. Leukotrienes C4 and D4 stimulate human endothelial cells to synthesize platelet-activating factor and bind neutrophils[J]. Proc Natl Acad Sci USA,1986,83:2204-2208.
[30]Nakashima Y, Raines EW, Plump AS, et al. Upregulation of VCAM-1 and ICAM-1 at atherosclerosis-prone sites on the endothelium in the ApoE-deficient mouse[J]. Arterioscler Thromb Vasc Biol,1998,18:842-851.
[31]Lessner SM, Prado HL, Waller EK, et al. Atherosclerotic lesions grow through recruitment and proliferation of circulating monocytes in a murine model [J]. Am J Pathol, 2002,160:2145-2155.
[32]Iiyama K, Hajra L, Iiyama M, et al. Patterns of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression in rabbit and mouse atherosclerotic lesions and at sites predisposed to lesion formation[J]. Circ Res,1999,85:199-207.
[33]Rosenfeld ME. Leukocyte recruitment into developing atherosclerotic lesions:the complex interaction between multiple molecules keeps getting more complex[J]. Arterioscler Thromb Vasc Biol,2003,22:361-363.
[34]Allen S, Khan S, Al-Mohanna F, Batten P, and Yacoub M. Native low density lipoprotein-induced calcium transients trigger VCAM-1 and E-selectin expression in cultured human vascular endothelial cells[J]. J Clin Invest,1998,101:1064-1075.
[35]Ley K. Molecular mechanisms of leukocyte recruitment in the inflammatory process[J]. Cardiovasc Res,1996,32:733-742.
[36]Weninger WJ, Muller GB, Reiter C, et al. Intimal hyperplasia of the infant parasellar carotid artery:a potential developmental factor in atherosclerosis and SIDS[J]. Circ Res, 1999,85:970-975.
[37]Stary HC. Natural history and histological classification of atherosclerotic lesions:an update[J]. Arterioscler Thromb Vasc Biol,2000,20:1177-1178.
[38]Ikari Y, McManus BM, Kenyon J, Schwartz SM. Neonatal intima formation in the human coronary artery [J]. Arterioscler Thromb Vasc Biol,1999,19:2036-2040.
[39]Schwartz SM, Murry CE. Proliferation and the monoclonal origins of atherosclerotic lesions[J]. Annu Rev Med,1998,49:437-460.
[40]Mosse PR, Campbell GR, Wang ZL, Campbell JH. Smooth muscle phenotypic expression in human carotid arteries. I. Comparison of cells from diffuse intimal thickenings adjacent to atheromatous plaques with those of the media[J]. Lab Invest,1985, 53:556-562.
[41]Worth NF, Rolfe BE, Song J, Campbell GR. Vascular smooth muscle cell phenotypic modulation in culture is associated with reorganisation of contractile and cytoskeletal proteins[J]. Cell Motil Cytoskeleton,2001,49:130-145.
[42]Thyberg J, Hultgardh-Nilsson A. Fibronectin and the basement membrane components laminin and collagen type IV influence the phenotypic properties of subcultured rat aortic smooth muscle cells differently[J]. Cell Tissue Res,1994, 276:263-271.
[43]Li X, Van Putten V, Zarinetchi F, et al. Suppression of smooth-muscle alpha-actin expression by platelet-derived growth factor in vascular smooth-muscle cells involves Ras and cytosolic phospholipase A2[J]. Biochem J,1997,327 (Pt 3):709-716.
[44]Reusch P, Wagdy H, Reusch R, et al. Mechanical strain increases smooth muscle and decreases nonmuscle myosin expression in rat vascular smooth muscle cells[J]. Circ Res, 1996,79:1046-1053.
[45]Su B, Mitra S, Gregg H, et al. Redox regulation of vascular smooth muscle cell differentiation[J]. Circ Res,2001,89:39-46.
[46]Pidkovka NA, Cherepanova OA, Yoshida T, et al. Oxidized phospholipids induce phenotypic switching of vascular smooth muscle cells in vivo and in vitro[J]. Circ Res, 2007,101:792-801.
[47]Ang AH, Tachas G, Campbell JH, et al. Collagen synthesis by cultured rabbit aortic smooth-muscle cells[J]. Alteration with phenotype. Biochem J,1990,265:461-469.
[48]Rong JX, Shapiro M, Trogan E, Fisher EA. Transdifferentiation of mouse aortic smooth muscle cells to a macrophage-like state after cholesterol loading[J]. Proc Natl Acad Sci U S A,2003,100:13531-13536.
[49]Ruan XZ, Moorhead JF, Tao JL, et al. Mechanisms of dysregulation of low-density lipoprotein receptor expression in vascular smooth muscle cells by inflammatory cytokines[J]. Arterioscler Thromb Vasc Biol,2006,26:1150-1155.
[50]Takahashi M, Takahashi S, Suzuki C, et al. IL-1 beta attenuates beta-very low-density lipoprotein uptake and its receptor expression in vascular smooth muscle cells[J]. J Mol Cell Cardiol,2005,38:637-646.
[51]Matsumoto K, Hirano K, Nozaki S, et al. Expression of macrophage (Mphi) scavenger receptor, CD36, in cultured human aortic smooth muscle cells in association with expression of peroxisome proliferator activated receptor-gamma, which regulates gain of Mphi-like phenotype in vitro, and its implication in atherogenesis[J]. Arterioscler Thromb Vasc Biol,2000,20:1027-1032.
[52]Wagsater D, Olofsson PS, Norgren L, et al. The chemokine and scavenger receptor CXCL16/SR-PSOX is expressed in human vascular smooth muscle cells and is induced by INF gamma[J]. Biochem Biophys Res Commun,2004,325:1187-1193.
[53]Botham KM, Bravo E, Elliott J, et al. Direct interaction of dietary lipids carried in chylomicron remnants with cells of the artery wall:implications for atherosclerosis development[J]. Curr Pharm Des,2005,11:3681-3695.
[54]Nagao S, Murao K, Imachi H, et al. Platelet derived growth factor regulates ABCA1 expression in vascular smooth muscle cells[J]. FEBS Lett,2006,580:4371-4376.
[55]Huo Y, Ley K. Adhesion molecules and atherogenesis[J]. Acta Physiol Scand,2001, 173:35-43.
[56]50. Braun M, Pietsch P, Schror K, et al. Cellular adhesion molecules on vascular smooth muscle cells[J]. Cardiovasc Res,1999,41:395-401.
[57]Cai Q, Lanting L, Natarajan R. Interaction of monocytes with vascular smooth muscle cells regulates monocyte survival and differentiation through distinct pathways[J]. Arterioscler Thromb Vasc Biol,2004,24:2263-2270.
[58]Jang Y, Lincoff AM, Plow ejectionfactor (EF), et al. Cell adhesion molecules in coronary artery disease[J]. J Am Coll Cardiol,1994,24:1591-1601.
[59]Endres M, Laufs U, Merz H, et al. Focal expression of intercellular adhesion molecule-1 in the human carotid bifurcation[J]. Stroke,1997,28:77-82.
[60]Wong BW, Wong D, McManus BM. Characterization of fractalkine (CX3CL1) and CX3CR1 in human coronary arteries with native atherosclerosis, diabetes mellitus, and transplant vascular disease[J]. Cardiovasc Pathol,2002,11:332-338.
[61]Barlic J, Zhang Y, Foley JF, et al. Oxidized lipid-driven chemokine receptor switch, CCR2 to CX3CR1, mediates adhesion of human macrophages to coronary artery smooth muscle cells through a peroxisome proliferator-activated receptor gamma-dependent pathway[J]. Circulation,2006,114:807-819.
[62]Barlic J, Zhang Y, Murphy PM. Atherogenic lipids induce adhesion of human coronary artery smooth muscle cells to macrophages by up-regulating chemokine CX3CL1 on smooth muscle cells in a TNFalpha-NF kappa B-dependent manner [J]. J Biol Chem, 2007,282:19167-19176.
[63]Isner JM, Kearney M, Bortman S, Passeri J. Apoptosis in human atherosclerosis and restenosis[J]. Circulation,1995,91:2703-2711.
[64]Raines EW, Ferri N. Thematic review series:The immune system and atherogenesis. Cytokines affecting endothelial and smooth muscle cells in vascular disease[J]. J Lipid Res, 2005,46:1081-1092.
[65]Engelberg H. Endogenous heparin activity deficiency:the'missing link'in atherogenesis? [J]. Atherosclerosis,2001,159:253-260.
[66]O'Brien KD, Olin KL, Alpers CE, et al. Comparison of apolipoprotein and proteoglycan deposits in human coronary atherosclerotic plaques:colocalization of biglycan with apolipoproteins[J]. Circulation,1998,98:519-527.
[67]Chait A, Wight TN. Interaction of native and modified low-density lipoproteins with extracellular matrix[J]. Curr Opin Lipidol,2000,11:457-463.
[68]Camejo G, Fager G, Rosengren B, Hurt-Camejo E, Bondjers G. Binding of low density lipoproteins by proteoglycans synthesized by proliferating and quiescent human arterial smooth muscle cells[J]. J Biol Chem,1993,268:14131-14137.
[69]Chang MY, Potter-Perigo S, Tsoi C, et al. Oxidized low density lipoproteins regulate synthesis of monkey aortic smooth muscle cell proteoglycans that have enhanced native low density lipoprotein binding properties [J]. J Biol Chem,2000,275:4766-4773.
[70]Bond M, Sala-Newby GB, Newby AC. Focal adhesion kinase (FAK)-dependent regulation of S-phase kinase-associated protein-2 (Skp-2) stability. A novel mechanism regulating smooth muscle cell proliferation[J]. J Biol Chem,2004,279:37304-37310.
[71]Koyama H, Raines EW, Bornfeldt KE, et al. Fibrillar collagen inhibits arterial smooth muscle proliferation through regulation of Cdk2 inhibitors[J]. Cell,1996,87:1069-1078.
[72]Roy J, Tran PK, Religa P, Kazi M, et al. Fibronectin promotes cell cycle entry in smooth muscle cells in primary culture[J]. Exp Cell Res,2002,273:169-177.
[73]Edwards IJ, Wagner WD. Distinct synthetic and structural characteristics of proteoglycans produced by cultured artery smooth muscle cells of atherosclerosis-susceptible pigeons[J]. J Biol Chem.1988;263: 9612-9620.
[74]Wight TN, Kinsella MG, Lark MW, et al. Vascular cell proteoglycans:evidence for metabolic modulation[J]. Ciba Found Symp,1986,124:241-259.
© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号 地址：北京市海淀区学院路29号 邮编：100083 电话：办公室：(+86 10)66554848；文献借阅、咨询服务、科技查新：66554700 |