Expression of leukocyte adhesion-related glycosyltransferase genes in acute coronary syndrome patients.

Inflamm Res

Internal Medicine Department, General Hospital "dr. Josip Benčević", Faculty of Medicine, University of Osijek, Andrije Štampara 42, 35000, Slavonski Brod, Croatia,

Published: August 2014

Introduction: Acute coronary syndrome (ACS) is caused by destabilization and rupture of atherosclerotic plaque in the coronary artery via mechanisms affecting leukocyte signaling, rolling, adhesion, extravasation and inflammation-promoting factors. The majority of cellular communication takes place on the membrane surface that is covered with glycoproteins and glycolipids synthesized by glycosyltransferases. The aim of this study was to determine the mRNA expression of leukocyte adhesion-related glycosyltransferases in patients during the onset and the chronic phase of ACS and to compare the expression with matching subjects without coronary disease.

Subjects And Methods: The study included 26 ACS patients and 26 ACS-free matched-pair controls. Blood samples were collected at the time of hospital admittance and 8 days later. Expression analysis of six fucosyltransferases and six sialyltransferases was performed by a real-time polymerase chain reaction.

Results: At the time of admittance ACS subjects had lower expression levels of FUT4, ST6GalNac4, ST6Gal1 and GM3 synthase (p < 0.05) than the control subjects, and moreover, after 8 days down-regulation of FUT7 and ST6GalNac3 was also observed (p < 0.05). When compared to the initial gene expression, after treatment and stabilization of ACS subjects, FUT7, ST6GalNac2 and ST6GalNac3 were down-regulated, whereas ST6GalNac1 was up-regulated. Expression levels of FUT7, ST6GalNac1, ST6GalNac2 and ST6GalNac3 were predicted by several drugs and medical history.

Conclusion: Expression of glycosyltransferase genes differs in ACS and control subjects. During the course of the ACS study we established further changes in gene expression levels. Medical history was predictive of gene expression levels while drugs were shown to modulate expression levels.

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http://dx.doi.org/10.1007/s00011-014-0735-3DOI Listing

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