| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on June 30, 2005
Accepted on November 16, 2005
From the Department of Pathology and Immunology (G.G., M.B., M.-L.B.-P.), University of Geneva-CMU, Geneva, Switzerland; Department of Pathology (H.H.), Hyogo Medical University, Hyogo, Japan; Division of Cardiology (E.C.), University Hospital Geneva, Geneva, Switzerland; CVPath (R.V.), International Registry of Pathology, Gaithersburg, Md.
* To whom correspondence should be addressed. E-mail: Marie-Luce.Piallat{at}medecine.unige.ch.
Objectives--Characterize the phenotypic features of media and intima coronary artery smooth muscle cells (SMCs) in mildly stenotic plaques, erosions, stable plaques, and in-stent restenosis.
Methods and Results--Expression of
-smooth muscle actin (
-SMA), smooth muscle myosin heavy chains (SMMHCs), and smoothelin was investigated by immunohistochemistry followed by morphometric quantification. The cross-sectional area and the expression of cytoskeletal proteins in the media were lower in restenotic lesions and, to a lesser extent, in stable plaques compared with mildly stenotic plaques and erosions. An important expression of
-SMA was detected in the intima of the different lesions; moreover,
-SMA staining was significantly larger in erosions compared with all other conditions. In the same location, a striking decrease of SMMHCs and a disappearance of smoothelin were observed in all situations.
Conclusions--Medial atrophy is prevalent in restenotic lesions and stable plaques compared with mildly stenotic plaques and erosions. Intimal SMCs of all situations exhibit a phenotypic profile, suggesting that they have modulated into myofibroblasts (MFs). The high accumulation of
-SMA-positive MFs in erosions compared with stable plaques correlates with the higher appearance of thrombotic complications in this situation.
-smooth muscle actin
erosion
smooth muscle myosin heavy chains
smoothelin
stable plaque
This article has been cited by other articles:
![]() |
M. Song, X. Yu, X. Cui, G. Zhu, G. Zhao, J. Chen, and L. Huang Blockade of Connexin 43 Hemichannels Reduces Neointima Formation After Vascular Injury by Inhibiting Proliferation and Phenotypic Modulation of Smooth Muscle Cells Experimental Biology and Medicine, October 1, 2009; 234(10): 1192 - 1200. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Gyongyosi, G. Christ, I. Lang, G. Kreiner, H. Sochor, P. Probst, T. Neunteufl, R. Badr-Eslam, S. Winkler, N. Nyolczas, et al. 2-Year Results of the AUTAX (Austrian Multivessel TAXUS-Stent) Registry: Beyond the SYNTAX (Synergy Between Percutaneous Coronary Intervention With TAXUS and Cardiac Surgery) Study J. Am. Coll. Cardiol. Intv., August 1, 2009; 2(8): 718 - 727. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Virmani, A. V. Finn, and F. D. Kolodgie Carotid Plaque Stabilization and Progression After Stroke or TIA Arterioscler Thromb Vasc Biol, January 1, 2009; 29(1): 3 - 6. [Full Text] [PDF] |
||||
![]() |
D. Morrow, S. Guha, C. Sweeney, Y. Birney, T. Walshe, C. O'Brien, D. Walls, E. M. Redmond, and P. A. Cahill Notch and Vascular Smooth Muscle Cell Phenotype Circ. Res., December 5, 2008; 103(12): 1370 - 1382. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Vaahtomeri, E. Ventela, K. Laajanen, P. Katajisto, P.-J. Wipff, B. Hinz, T. Vallenius, M. Tiainen, and T. P. Makela Lkb1 is required for TGF{beta}-mediated myofibroblast differentiation J. Cell Sci., November 1, 2008; 121(21): 3531 - 3540. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. S. Rensen, P. M. Niessen, J. M. van Deursen, B. J. Janssen, E. Heijman, E. Hermeling, M. Meens, N. Lie, M. J. Gijbels, G. J. Strijkers, et al. Smoothelin-B Deficiency Results in Reduced Arterial Contractility, Hypertension, and Cardiac Hypertrophy in Mice Circulation, August 19, 2008; 118(8): 828 - 836. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Han, J. Deng, L. Guo, C. Yan, M. Liang, J. Kang, H. Liu, A. M. Graham, and S. Li CREG promotes a mature smooth muscle cell phenotype and reduces neointimal formation in balloon-injured rat carotid artery Cardiovasc Res, June 1, 2008; 78(3): 597 - 604. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Borensztajn, J. Stiekema, S. Nijmeijer, P. H. Reitsma, M. P. Peppelenbosch, and C. A. Spek Factor Xa Stimulates Proinflammatory and Profibrotic Responses in Fibroblasts via Protease-Activated Receptor-2 Activation Am. J. Pathol., February 1, 2008; 172(2): 309 - 320. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. K. Cheruvu, A. V. Finn, C. Gardner, J. Caplan, J. Goldstein, G. W. Stone, R. Virmani, and J. E. Muller Frequency and Distribution of Thin-Cap Fibroatheroma and Ruptured Plaques in Human Coronary Arteries: A Pathologic Study J. Am. Coll. Cardiol., September 4, 2007; 50(10): 940 - 949. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Hinz, S. H. Phan, V. J. Thannickal, A. Galli, M.-L. Bochaton-Piallat, and G. Gabbiani The Myofibroblast: One Function, Multiple Origins Am. J. Pathol., June 1, 2007; 170(6): 1807 - 1816. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. C. Brisset, H. Hao, E. Camenzind, M. Bacchetta, A. Geinoz, J.-C. Sanchez, C. Chaponnier, G. Gabbiani, and M.-L. Bochaton-Piallat Intimal Smooth Muscle Cells of Porcine and Human Coronary Artery Express S100A4, a Marker of the Rhomboid Phenotype In Vitro Circ. Res., April 13, 2007; 100(7): 1055 - 1062. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Virmani, A. P. Burke, A. Farb, and F. D. Kolodgie Pathology of the vulnerable plaque. J. Am. Coll. Cardiol., April 18, 2006; 47(8 Suppl): C13 - C18. [Abstract] [Full Text] [PDF] |
||||
![]() |
M.-L. Bochaton-Piallat and G. Gabbiani Smooth Muscle Cell: A Key Cell for Plaque Vulnerability Regulation? Circ. Res., March 3, 2006; 98(4): 448 - 449. [Full Text] [PDF] |
||||
|
ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2005 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |