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Thromb Haemost 2001; 85(05): 793-799
DOI: 10.1055/s-0037-1615720
Review Article
Schattauer GmbH

Plasma Levels of Syndecan-4 (Ryudocan) Are Elevated in Patients with Acute Myocardial Infarction

Tetsuhito Kojima
1   Department of Medical Technology, Nagoya University School of Health Sciences
2   First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya
,
Akira Takagi
1   Department of Medical Technology, Nagoya University School of Health Sciences
,
Masahiro Maeda
3   Immuno-Biological Laboratories, Co. Ltd., Fujioka
,
Tatsuya Segawa
3   Immuno-Biological Laboratories, Co. Ltd., Fujioka
,
Atsuya Shimizu
2   First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya
,
Koji Yamamoto
2   First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya
,
Tadashi Matsushita
2   First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya
,
Hidehiko Saito
2   First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya
4   Aichi Juridical Foundation for Blood Disease Research, Nagoya, Japan
› Author Affiliations
Further Information

Publication History

Received 06 June 2000

Accepted after resubmission 02 January 2001

Publication Date:
11 December 2017 (online)

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Summary

Syndecan-4 (ryudocan) is a cell-surface heparan sulfate proteoglycan, which plays an important role in a variety of biological functions including regulation of blood coagulation, cell adhesion, and cell growth. In this study, we measured plasma levels of syndecan-4 in patients with acute myocardial infarction using an enzyme-immunoassay, and found that they were extremely high, with a peak of average (10.5 ± 5.6 ng/ml, 2 weeks after onset), as compared with those in normal subjects (0.078 ± 0.030 ng/ml) (p < 0.001). We also observed a distinct expression of syndecan-4 in the repair region of the damaged cardiac tissues with infarction, but not in intact region, by immunohistochemical analysis. To clarify the mechanism of syndecan-4 induction, we investigated the hypoxia effect on its expression, and found that hypoxia treatment up-regulated the gene expression of syndecan-4 in various types of cells. Taken together, it is suggested that syndecan-4 is induced by hypoxia stimuli in ischemic heart tissues, and may function as a tissue-repair molecule via biological mediators such as heparin-binding growth factors.

Keywords

Syndecan-4 (ryudocan) - enzyme-linked immuno-sorbent assay (ELISA) - acute myocardial infarction - hypoxia - tissue repair
 

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