The significance of −786T > C polymorphism of endothelial NO synthase (eNOS) gene in severe preeclampsia

Abstract

Objective. Preeclampsia (PE) is believed to be induced by endothelial cell dysfunction in placenta. Highly polymorphic endothelial nitric oxide synthase (eNOS) activity belongs to the factors significantly influencing vaso-motor tone in placenta and PE susceptibility. The aim of this study was to evaluate prevalence of −786T/C polymorphism of eNOS gene in the groups of women with mild and severe PE.

Study design. The study was performed in the group of 218 preeclamptic (including 136 with severe PE) and of 400 normotensive healthy women delivered normally after a healthy gestation. The eNOS −786T/C polymorphism was determined using PCR/RFLP assay. Additionally, detailed correlation between eNOS genotypes and clinical/laboratory data in the PE group has been analyzed.

Results. The higher frequency of mutated homozygous CC genotypes (17.4% vs. 11.5% in controls, OR 1.62, n.s.) and of C alleles (allelic frequency 44.1 vs. 36.6%; OR 1.36, p = 0.012) in the group of PE has been determined. Furthermore, in the group of severe PE the overrepresentation of mutated CC genotypes (23.5% vs. 11.5%, OR 2.37, p = 0.0014) and mutated C alleles (47.8 vs. 36.6%, OR 1.58, p = 0.0016) has been found.

Conclusions. The presence of mutated homozygous CC genotype and C allele of −786T/C polymorphism of eNOS gene influences the higher susceptibility to develop severe PE development.

Keywords:

• Preeclampsia
• endothelial nitric oxide synthase
• genetic polymorphism

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.