Balkan Journal of Medical Genetics

AN INVESTIGATION OF THE RELATIONSHIP BETWEEN THE eNOS GENE POLYMORPHISM AND DIAGNOSED MIGRAINE
Güler S1,*, Gürkan H2, Tozkir H2, Turan N3, Çelik Y1
*Corresponding Author: Sibel Güler, M.D., Department of Neurology, Trakya University Faculty of Medicine, Balkan Yerleşkesi, 22030 Edirne, Turkey. Tel: +90-284-236-49-81. Fax: +90-284-223-42-03. E-mail: drsibleguler@ yahoo.com
page: 49

INTRODUCTION

Migraine is a neurological disease that affects approximately 12.0-16.0% of the population. It leads to specific disabling conditions and has a genetic component [1]. Despite its high prevalence, the complex pathogenetic mechanisms of migraine remain unclear. However, the significance of nitric oxide (NO) in migraine pathogenesis has been reported in some studies. In essence, NO plays an important role in cerebral blood flow regulation and is involved in the activation of nociceptors in the trigeminovascular system and the release of vasoactive neuropep-tides during the neurogenic inflammatory response [2,3] causing vascular homeostasis, blocking of platelet adhesion and aggregation, inhibition of migration and proliferation of leukocyte and vascular muscle cells [4]. Thus, NO makes a significant contribution to antiatherogenic features in the endothelium. According to recent studies, genes encoding endothelial function regulators are indicated as significant candidate genes in individuals susceptible to migraine. Therefore, it has been claimed that gene polymorphisms for endothelial nitric oxide synthase gene (eNOS), are possible genetic factors involved in migraine [2]. It has been indicated that there is a strong association between NO and the pathophysiology of migraine and aura [5]. During the headache phase, an increase of platelets and administration of NO as an exogen makes the headache worse [5]. A Glu 268Asp amino acid change and point mutation (G894T, rs1799983) leads to a guanine to thymine change on exon 7 and nucleotide (nt) 894 in the eNOS gene, and this is related to reduced basal NO production. Another polymorphism (–786T>C, rs1800779) leads to a thymine to cytosine change on the eNOS 5’ promoter region –786 nt, which causes a reduction of both eNOS gene promoter activity and basal NO production [2]. To date, the studies investigating the association between migraine and eNOS gene polymorphisms have focused on eNOS rs743506, rs2070744, rs1799983, rs180079, rs3918226, rs207468799 and rs148554851 [5]. We believe that it is important to determine the genetic basis of the common primary headache that leads to migraine, since the latter creates disabling circumstances for people with regard to their social and working life. Therefore, we investigated phenotype- genotype association between eNOS rs743506, rs2070744, rs1799983, rs180079, rs3918226, rs207468799 and rs148554851 gene polymorphisms, which we suggest are candidate markers of susceptibility to migraine with and without aura.

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