Open Access Research Article

Investigation of Leptin Receptor and eNOS Gene Polymorphisms in Preeclamptic Umbilical Cords

Fatma Secer Celik1*, Esra Celen1,4, Hatice Kubra Yildiz1, Safaa Altweish1, Huseyin Donmez1, Yasemin Gurbuz1, Ayten Demirci2, Esra Buyuk2, Esra Un Arslan,2, Merve Ilhan3, Ayse Saide Sahin2 and Hasibe Vural1

1Department of Medical Biology, Necmettin Erbakan University, Turkey

2Department of Medical Pharmacology, Necmettin Erbakan University, Turkey

3Department of Medical Biochemistry, Necmettin Erbakan University, Turkey

4Faculty of Agriculture and Natural Sciences, Konya Food and Agriculture University, Turkey

Corresponding Author

Received Date: November 27, 2018;  Published Date: December 06, 2018


Background: Preeclampsia occurs in the umbilical artery with proteinuria and edema accompanying pregnancy-induced hypertension. Vasoconstriction results in severe complications such as intrauterine growth restriction, preterm birth, fetal death due to decreased uteroplacental blood flow. Preeclampsia may cause perinatal mortality and morbidity and it is one of the most important causes of maternal mortality. The etiology and pathogenesis of preeclampsia, which is present in 7,18% of all pregnancies, has not yet been elucidated. However, it is thought that one of the causes of pathogenesis may be caused by possible changes in the synthesis of endothelial nitric oxide synthase (eNOS) mediated nitric oxide (NO). DNA sequencing studies revealed many single nucleotide polymorphisms (SNPs) in the promoter region, exons and introns of this gene. T-786C SNP is found in the promoter region of the eNOS gene. There are several agents affecting eNOS activity in preeclampsia. Leptin is one of these agents. The exact reason of why leptin, which is a vasodilator agent, has no effect on preeclamptic pregnancies, is not known yet. However, it is thought that the leptin receptor gene Lys109Arg SNP in exon4 and Gly223Arg SNP in exon6 may affect receptor function and signaling.

Materials and methods: We investigated polymorphisms of eNOS and leptin receptor genes with HRM and PCR-RFLP techniques.

Results: Both analyses showed no SNPs in exon4 of leptin receptor (LEPR) gene in preeclampsia patients suggesting that there should be no relationship with exon4 of LEPR gene and preeclampsia. We found that there were SNPs in promoter region of eNOS gene and exon6 of LEPR gene.

Conclusion: HRM and PCR-RFLP gave different number of SNPs, these SNPs of these genes could be related with preeclampsia. This study is a preliminary step for our next molecular studies although few numbers of the samples were included. Increasing the number of samples would give the statistically significant results.

Keywords: Leptin, Preeclampsia, Polymorphism

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