Coker-Gurkan Ajda, Coskun Deniz, Arisan Elif Damla, Obakan Pinar, Soylu Özer, Unsal Narcin Palavan
Department of Molecular Biology and Genetics, Istanbul Kultur University, Atakoy Campus, Istanbul 34156, Turkey.
Heart and Vessel Surgery Department, Medical Park Hospital, Istanbul 34732, Turkey.
Mol Med Rep. 2015 Jul;12(1):1356-62. doi: 10.3892/mmr.2015.3521. Epub 2015 Mar 20.
Inflammation and genetics have key roles in the pathogenesis of atherosclerosis, and the etiology of myocardial infarction (MI). Recent studies have indicated that lower serum levels of fetuin-A may accelerate the vascular mineralization process, which leads to pathophysiological conditions, such as coronary heart disease and chronic renal failure. The aim of the present study was to evaluate the association between specific fetuin-A polymorphisms (742 and 766) that are associated with circulating serum levels, and MI cases. The study consisted of 292 participants; 146 healthy control subjects and 146 patients with MI. The patient group was divided into two subgroups: 56 MI ≤ 40 years and 90 MI ≥ 40 years. The genotype distribution of fetuin 742 (C/T) and fetuin 766 (C/G) were determined by restriction enzyme digestion of polymerase chain reaction products. A significant difference was determined between the patients with MI and the control subjects with regards to fetuin-A 742 C/T gene polymorphism (P=0.028), regardless of age. Genotype distributions of fetuin-A 742 (C/G, P=0.004) and 766 (C/T, P=0.017) were statistically different in the older patients with MI (MI ≥ 40 years old), as compared with the healthy controls; however, there were no significant differences between the younger patients with MI and the controls, with regards to fetuin-A 742 C/T (P=0.519) and 766 C/G (P=0.653) gene polymorphisms. In addition, an association was observed between the presence of fetuin-A 742 T and 766 G alleles, and MI cases. The present study demonstrates that fetuin-A 742 (C/T) and 766 (C/G) genotypes may be risk factors for MI in patients older than 40 years of age.
炎症和遗传因素在动脉粥样硬化及心肌梗死（MI）的发病机制中起着关键作用。最近的研究表明，较低的血清胎球蛋白-A水平可能会加速血管矿化过程，从而导致诸如冠心病和慢性肾衰竭等病理生理状况。本研究的目的是评估与循环血清水平相关的特定胎球蛋白-A多态性（742和766）与心肌梗死病例之间的关联。该研究包括292名参与者；146名健康对照者和146名心肌梗死患者。患者组分为两个亚组：56名年龄≤40岁的心肌梗死患者和90名年龄≥40岁的心肌梗死患者。通过聚合酶链反应产物的限制性酶切来确定胎球蛋白742（C/T）和胎球蛋白766（C/G）的基因型分布。无论年龄大小，心肌梗死患者与对照者在胎球蛋白-A 742 C/T基因多态性方面存在显著差异（P=0.028）。与健康对照者相比，年龄较大的心肌梗死患者（年龄≥40岁）中胎球蛋白-A 742（C/G，P=0.004）和766（C/T，P=0.017）的基因型分布在统计学上有差异；然而，年龄较小的心肌梗死患者与对照者在胎球蛋白-A 742 C/T（P=0.519）和766 C/G（P=0.653）基因多态性方面没有显著差异。此外，观察到胎球蛋白-A 742 T和766 G等位基因的存在与心肌梗死病例之间存在关联。本研究表明，胎球蛋白-A 742（C/T）和766（C/G）基因型可能是40岁以上患者发生心肌梗死的危险因素。
