Fibrous cap formation or destruction - the critical importance of vascular smooth muscle cell proliferation, migration and matrix formation

被引:263
作者
Newby, AC [1 ]
Zaltsman, AB [1 ]
机构
[1] Univ Bristol, Bristol Royal Infirm, British Heart Inst, Bristol BS2 8HW, Avon, England
基金
英国医学研究理事会;
关键词
arteriosclerosis; vascular smooth muscle; extracellular matrix; metalloproteinases;
D O I
10.1016/S0008-6363(98)00286-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Endothelial activation and infiltration of monocyte macrophages are essential prerequisites for fibrous cap formation, which comprises proliferation and migration of smooth muscle cells and net matrix deposition. Macrophage foam cells and endothelium act as a sourer of growth factors and chemoattractants for smooth muscle cells. However, growth factors alone do not stimulate smooth muscle cell proliferation or migration. This requires, in addition, the remodelling of the extracellular matrix, at least partly mediated by metalloproteinases. Tn particular, loss of basement membrane components and contact with the interstitial matrix appears to be required to release a brake on proliferation and migration exerted by the basement membrane. Unless there is a change in the phenotype of macrophages in advanced lesions, it is not clear why fibrous cap destruction rather than formation should take place in macrophage-rich shoulder regions of plaques. Impaired cap formation caused by smooth muscle senescence, mummification and propensity to apoptosis may be as important as increased cap destruction in promoting plaque rupture. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:345 / 360
页数:16
相关论文
共 221 条
  • [1] SIGNALING MECHANISMS IN THE REGULATION OF VASCULAR CELL-MIGRATION
    ABEDI, H
    ZACHARY, I
    [J]. CARDIOVASCULAR RESEARCH, 1995, 30 (04) : 544 - 556
  • [2] Effect of immunization with homologous LDL and oxidized LDL on early atherosclerosis in hypercholesterolemic rabbits
    Ameli, S
    HultgardhNilsson, A
    Regnstrom, J
    Calara, F
    Yano, J
    Cercek, B
    Shah, PK
    Nilsson, J
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1996, 16 (08) : 1074 - 1079
  • [3] COLLAGEN-SYNTHESIS BY CULTURED RABBIT AORTIC SMOOTH-MUSCLE CELLS - ALTERATION WITH PHENOTYPE
    ANG, AH
    TACHAS, G
    CAMPBELL, JH
    BATEMAN, JF
    CAMPBELL, GR
    [J]. BIOCHEMICAL JOURNAL, 1990, 265 (02) : 461 - 469
  • [4] Angelini G D, 1991, Eur J Vasc Surg, V5, P5, DOI 10.1016/S0950-821X(05)80919-3
  • [5] ANGELINI GD, 1992, J THORAC CARDIOV SUR, V103, P1093
  • [6] Anitschkow N, 1913, ZENTRALBL ALLG PATHO, V24, P1
  • [7] IDENTIFICATION OF MACROPHAGES AND SMOOTH-MUSCLE CELLS IN HUMAN ATHEROSCLEROSIS USING MONOCLONAL-ANTIBODIES
    AQEL, NM
    BALL, RY
    WALDMANN, H
    MITCHINSON, MJ
    [J]. JOURNAL OF PATHOLOGY, 1985, 146 (03) : 197 - 204
  • [8] INHIBITION OF PROLIFERATION, BUT NOT OF CA-2+ MOBILIZATION, BY CYCLIC-AMP AND GMP IN RABBIT AORTIC SMOOTH-MUSCLE CELLS
    ASSENDER, JW
    SOUTHGATE, KM
    HALLETT, MB
    NEWBY, AC
    [J]. BIOCHEMICAL JOURNAL, 1992, 288 : 527 - 532
  • [9] HEPARIN DECREASES ACTIVATOR PROTEIN-1 BINDING TO DNA IN PART BY POSTTRANSLATIONAL MODIFICATION OF JUN-B
    AU, YPT
    DOBROWOLSKA, G
    MORRIS, DR
    CLOWES, AW
    [J]. CIRCULATION RESEARCH, 1994, 75 (01) : 15 - 22
  • [10] Divergent effects of tissue inhibitor of metalloproteinase-1, -2, or -3 overexpression on rat vascular smooth muscle cell invasion, proliferation, and death in vitro - TIMP-3 promotes apoptosis
    Baker, AH
    Zaltsman, AB
    George, SJ
    Newby, AC
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (06) : 1478 - 1487