IL-27 variants might be genetic risk factors for preeclampsia: based on genetic polymorphisms, haplotypes and in silico
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ORIGINAL ARTICLE
IL‑27 variants might be genetic risk factors for preeclampsia: based on genetic polymorphisms, haplotypes and in silico approach Danial Jahantigh1 · Saeedeh Ghazaey Zidanloo2 · Forough Forghani3,4 · Mohammad Doroudian5 Received: 4 August 2020 / Accepted: 28 September 2020 © Springer Nature B.V. 2020
Abstract Pre-eclampsia (PE) is a disorder that occurs only during pregnancy. PE is associated with neonate mortality and morbidity. Overexpression of IL-27 and its receptor have been reported frequently in the trophoblast cells of patients with PE. In this study, we aimed to evaluate the relationship between genetic polymorphisms of IL-27 rs153109, and rs17855750 in an Iranian cohort of 170 PE patients and 170 normal pregnant women using the PCR-RFLP method. In the total PE, the frequency of heterozygous and mutant homozygous genotypes of rs153109 was significantly higher, severe, and mild PE groups. The genotypes and alleles frequencies of rs17855750 gene polymorphism were associated with PE susceptibility in total, severe and early-onset sub-group patients. Haplotype analysis of IL-27 rs153109 and rs17855750 polymorphisms revealed that the mutant GG haplotype frequencies significantly increased the risk of preeclampsia in total PE and different sub-group patients, while the wild AT haplotypes were associated with decreased risk of pre-eclampsia in total and sub-group patients. The in-silico analysis showed the transition of allele A to allele G in rs153109 SNP, would lead to create a new binding site and consequently may lead to changes in IL-27 gene expression. We found that rs17855750 A>G polymorphism might be influence the function of IL-27 protein. The data attained in our study propose the incidence of IL-27rs153109 and rs17855750 SNPs might be capable to be utilized as indicators for the genetic susceptibility to PE. Keywords IL-27 · Preeclampsia · Genetic polymorphism · In-silico · Post translational modification
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11033-020-05871-z) contains supplementary material, which is available to authorized users. * Forough Forghani [email protected] * Mohammad Doroudian [email protected] 1
Department of Biology, Faculty of Science, University of Sistan and Baluchestan, Zahedan, Iran
2
Department of Cell and Molecular Biology, Kosar University of Bojnord, Bojnord, Iran
3
Department of Obstetrics and Gynecology, Faculty of Medicine, Zabol University of Medical Sciences, Zabol, Iran
4
Department of Obstetrics and Gynecology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran
5
Department of Cell and Molecular Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran
Abbreviations PE Preeclampsia IL Interleukin TNF-α Tumor necrosis factor alpha IFN-γ Interferon gamma Th1 T helper type 1 Th2 T helper type 2 EBI3 Epstein-barr virus induced 3 TGF-β1 Transforming growth factor beta 1 PCR Polymerase chain reaction RFLP Restriction frag
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