ArticleMolecular and cellular biochemistry2012
Increased level of soluble syndecan-1 in serum correlates with myocardial expression in a rat model of myocardial infarction.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Identification of Hub Genes in the Remodeling of Non-Infarcted Myocardium Following Acute Myocardial Infarction.Journal of cardiovascular development and disease · 2022Article
- The Role of Matrix Proteins in Cardiac Pathology.International journal of molecular sciences · 2022Review
- HDAC3 Downregulation Improves Cerebral Ischemic Injury via Regulation of the SDC1-Dependent JAK1/STAT3 Signaling Pathway Through miR-19a Upregulation.Molecular neurobiology · 2021Article
- Soluble syndecans: biomarkers for diseases and therapeutic options.British journal of pharmacology · 2019Review
- Myofibroblasts and the extracellular matrix network in post-myocardial infarction cardiac remodeling.Pflugers Archiv : European journal of physiology · 2014Review
- Sdc1 overexpression inhibits the p38 MAPK pathway and lessens fibrotic ventricular remodeling in MI rats.Inflammation · 2013Article
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Authors and funding
7 authors.
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Abstract
A candidate marker for ventricular remodeling after myocardial infarction (MI), syndecan-1 (Sdc1), has been shown to be upregulated in myocardial tissues. However, the clinical potential of this marker depends on the ability to obtain samples safely and noninvasively. Therefore, we investigated the expression of soluble Sdc1 in the serum of rats after MI. Anterior descending coronary arteries of Sprague-Dawley rats were ligated, and MI was confirmed by morphologic and physiologic methods. Rats that underwent surgery without ligation served as the control group. We analyzed the expression of Sdc1 mRNA by quantitative reverse-transcription polymerase chain reaction and that of Sdc1 protein by western blot in heart tissue from the MI border and compared it to the expression of soluble Sdc1 in serum. The myocardial levels of expression of Sdc1 mRNA and protein were very low in the sham group but increased significantly in the MI group (P<0.01). The expression of myocardial Sdc1 reached a peak at day 3 and declined gradually thereafter, although the levels at 14 days remained significantly higher than those in the sham group. The expression of soluble Sdc1 in the sera of the rats in the MI group followed a similar pattern and was linearly correlated with the expression of Sdc1 protein in the MI border zone (r=0.952, P<0.01). Soluble Sdc1 was also detected at low levels in normal rat serum. These results may facilitate additional exploration of the utility of serum Sdc1 as a biomarker for MI in humans.
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