Expression of cartilage-specific markers in calcified and non-calcified atherosclerotic lesions

被引:16
作者
Aigner, Thomas [1 ]
Neureiter, Daniel [2 ]
Campean, Valentina [3 ]
Soder, Stephan [1 ]
Amann, Kerstin [3 ]
机构
[1] Univ Leipzig, Inst Pathol, D-04103 Leipzig, Germany
[2] Salzburg Univ, Dept Pathol, A-5020 Salzburg, Austria
[3] Univ Erlangen Nurnberg, Dept Pathol, D-8520 Erlangen, Germany
关键词
cartilage; chondrogenesis; artery; myocytes; collagen;
D O I
10.1016/j.atherosclerosis.2007.01.020
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Recently, molecular mechanisms resembling endochondral ossification were suggested to be important for atherosclerotic vessel calcification. The aim of this study was to investigate in a series of human atherosclerotic (non-diabetic) lesions of the crural arteries the distribution and expression of classical marker genes of the endochondral ossification pathway. Immunostaining for marker proteins S-100 protein and collagen types II and X were performed on atherosclerotic lesions of different grades (according to Stary). Quantitative real-time PCR for human COL1A1, COL2A1, COL10A1, SOX9, and BMP-2 was applied on RNA isolated from atherosclerotic arteries. In most samples, no expression of collagen type II and S-100 protein was found. Exceptionally, S-100 protein and type II collagen expression was observed very focally within advanced atherosclerotic plaques. Type X collagen was not detected in any of the lesions investigated. Overall, in our study we found no evidence that chondrogenic differentiation pathways are generally active in atherosclerotic plaque formation. In particular type X collagen, one important molecule in cartilage calcification, was not expressed in any of the investigated specimens. Occasionally, however, chondrocytic differentiation markers occur within atherosclerotic lesions. This most likely represents a metaplastic event associated, but not causative for atherosclerotic vessel degeneration and calcification. (C) 2007 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:37 / 41
页数:5
相关论文
共 24 条
[1]   Mesenchymal stem cells and the artery wall [J].
Abedin, M ;
Tintut, Y ;
Demer, LL .
CIRCULATION RESEARCH, 2004, 95 (07) :671-676
[2]   Cell differentiation and matrix gene expression in mesenchymal chondrosarcomas [J].
Aigner, T ;
Loos, S ;
Müller, S ;
Sandell, LJ ;
Unni, KK ;
Kirchner, T .
AMERICAN JOURNAL OF PATHOLOGY, 2000, 156 (04) :1327-1335
[3]   A transcriptional regulator of osteogenesis expressed in calcifying atherosclerotic plaques [J].
Brindle, NPJ .
CARDIOVASCULAR RESEARCH, 2001, 52 (02) :178-180
[4]   Differential expression of bone matrix regulatory proteins in human atherosclerotic plaques [J].
Dhore, CR ;
Cleutjens, JPM ;
Lutgens, E ;
Cleutjens, KBJM ;
Geusens, PPM ;
Kitslaar, PJEHM ;
Tordoir, JHM ;
Spronk, HMH ;
Vermeer, C ;
Daemen, MJAP .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2001, 21 (12) :1998-2003
[5]   Calcification in atherosclerosis: Bone biology and chronic inflammation at the arterial crossroads [J].
Doherty, TM ;
Asotra, K ;
Fitzpatrick, LA ;
Qiao, JH ;
Wilkin, DJ ;
Detrano, RC ;
Dunstan, CR ;
Shah, PK ;
Rajavashisth, TB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (20) :11201-11206
[6]   Rationale for the role of osteoclast-like cells in arterial calcification [J].
Doherty, TM ;
Uzui, H ;
Fitzpatrick, LA ;
Tripathi, PV ;
Dunstan, CR ;
Asotra, K ;
Rajavashisth, TB .
FASEB JOURNAL, 2002, 16 (06) :577-582
[7]   Bone morphogenetic protein-2 (BMP-2) inhibits muscle development and promotes cartilage formation in chick limb bud cultures [J].
Duprez, DM ;
Coltey, M ;
Amthor, H ;
Brickell, PM ;
Tickle, C .
DEVELOPMENTAL BIOLOGY, 1996, 174 (02) :448-452
[8]   Recombinant bone morphogenetic protein (BMP)-2 regulates costochondral growth plate chondrocytes and induces expression of BMP-2 and BMP-4 in a cell maturation-dependent manner [J].
Erickson, DM ;
Harris, SE ;
Dean, DD ;
Harris, MA ;
Wozney, JM ;
Boyan, BD ;
Schwartz, Z .
JOURNAL OF ORTHOPAEDIC RESEARCH, 1997, 15 (03) :371-380
[9]   Atherosclerotic vascular disease conference - Writing group III: Pathophysiology [J].
Faxon, DP ;
Fuster, V ;
Libby, P ;
Beckman, JA ;
Hiatt, WR ;
Thompson, RW ;
Topper, JN ;
Annex, BH ;
Rundback, JH ;
Fabunmi, RP ;
Robertson, RM ;
Loscalzo, J .
CIRCULATION, 2004, 109 (21) :2617-2625
[10]   Endochondral bone formation in the heart: A possible mechanism of coronary calcification [J].
Fitzpatrick, LA ;
Turner, RT ;
Ritman, ER .
ENDOCRINOLOGY, 2003, 144 (06) :2214-2219