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1 Ullevaal University Hospital, Institute for Experimental Medical Research, Oslo, Norway
2 Ullevaal University Hospital, Institute for Experimental Medical Research, Oslo, Norway; Department of Cardiothoracic Surgery, Ullevaal University Hospital, Oslo, Norway
3 Beth Israel Deaconess Medical Center, Harvard Medical School, Cardiovascular Division, Boston, USA
4 Research Forum, Ullevaal University Hospital, Oslo, Norway
* To whom correspondence should be addressed. E-mail: alexandra.finsen{at}ioks.uio.no.
The purpose of this study was to identify essential genes involved in myocardial growth and remodeling following myocardial infarction (MI). Left ventricular non-infarcted tissues from six mice subjected to MI under general anesthesia and from six sham operated mice were obtained one week after primary surgery, and analyzed by means of cDNA filter arrays. Out of a total of 1176 genes, 641 were consistently expressed, twenty-three were upregulated and thirteen downregulated. Five genes were only expressed following MI. Syndecan-3, a transmembranous heparan sulphate 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 1-4, 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 non-infarcted left ventricular tissue following MI,including syndecan 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.
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