Internal Medicine Department, General Hospital "dr. Josip Benčević", Faculty of Medicine, University of Osijek, Andrije Štampara 42, 35000, Slavonski Brod, Croatia,
Inflamm Res. 2014 Aug;63(8):629-36. doi: 10.1007/s00011-014-0735-3. Epub 2014 Apr 19.
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.
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.
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.
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.
急性冠状动脉综合征（ACS）是由于冠状动脉粥样硬化斑块的不稳定和破裂引起的，其机制涉及白细胞信号转导、滚动、黏附、渗出和炎症促进因素。大多数细胞间的通讯发生在细胞膜表面，该表面覆盖着糖基转移酶合成的糖蛋白和糖脂。本研究旨在确定白细胞黏附相关糖基转移酶在 ACS 发病期和慢性期患者中的 mRNA 表达，并将其与无冠心病的匹配对照进行比较。
该研究纳入了 26 例 ACS 患者和 26 例 ACS 对照组患者。在入院时和 8 天后采集血液样本。通过实时聚合酶链反应分析 6 种岩藻糖基转移酶和 6 种唾液酸转移酶的表达。
入院时，ACS 患者的 FUT4、ST6GalNac4、ST6Gal1 和 GM3 合酶的表达水平低于对照组（p<0.05），此外，8 天后还观察到 FUT7 和 ST6GalNac3 的下调（p<0.05）。与初始基因表达相比，ACS 患者经治疗和稳定后，FUT7、ST6GalNac2 和 ST6GalNac3 下调，而 ST6GalNac1 上调。FUT7、ST6GalNac1、ST6GalNac2 和 ST6GalNac3 的表达水平可由多种药物和病史预测。
ACS 患者和对照组患者的糖基转移酶基因表达不同。在 ACS 研究过程中，我们发现基因表达水平进一步发生变化。病史可预测基因表达水平，而药物可调节表达水平。
