Increased syndecan expression following myocardial infarction indicates a role in cardiac remodeling

被引:41
作者
Finsen, AV
Woldbaek, PR
Li, J
Wu, JP
Lyberg, T
Tonnessen, T
Christensen, G
机构
[1] Ullevaal Univ Hosp, Expt Med Res Inst, N-0407 Oslo, Norway
[2] Ullevaal Univ Hosp, Dept Cardiothorac Surg, N-0407 Oslo, Norway
[3] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Cardiovasc, Boston, MA 02215 USA
[4] Ullevaal Univ Hosp, Res Forum, N-0407 Oslo, Norway
关键词
extracellular matrix; gene expression; hypertrophy;
D O I
10.1152/physiolgenomics.00144.2002
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The purpose of this study was to identify essential genes involved in myocardial growth and remodeling following myocardial infarction (MI). Left ventricular noninfarcted tissues from six mice subjected to MI under general anesthesia and from six sham-operated mice were obtained 1 wk after primary surgery and analyzed by means of cDNA filter arrays. Out of a total of 1,176 genes, 641 were consistently expressed, twenty-three were upregulated and thirteen downregulated. Five genes were only expressed following MI. Syndecan-3, a transmembranous heparan sulfate proteoglycan, was found to be upregulated together with a transcriptional activator of syndecans, Wilms tumor protein 1 (WT-1). Northern blotting demonstrated a significant upregulation of syndecan-1, -2, -3, and -4, WT-1, fibronectin, and basic fibroblast growth factor (FGF) receptor 1. Furthermore, Western blot analysis showed statistically significant increases in protein levels for syndecan-3 and -4. In conclusion, we have identified a subset of genes with increased expression in noninfarcted left ventricular tissue following MI, including syndecans 1-4, WT-1, fibronectin, collagen 6A, and FGF receptor 1. Since the syndecans link the cytoskeleton to the extracellular matrix and function as required coreceptors for FGF, we suggest a role for the syndecans in cardiac remodeling following MI.
引用
收藏
页码:301 / 308
页数:8
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