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Preeclampsia (PE) is a pregnancy-specific complication which is a major cause of maternal and fetal morbidity and mortality. Recent studies have shown the aberrant expression of microRNAs (miRNAs) in the placenta of patients with PE. Dicer1 is a key enzyme in the generation of small noncoding RNAs including miRNAs. The aim of this study is to investigate the relationship between maternal and placental Dicer1 rs3742330 polymorphism and placental Dicer1 mRNA expression in PE and normotensive pregnant women. The blood and placenta of PE pregnant and normotensive pregnant women were collected after delivery. Dicer1 rs3742330 polymorphism was genotyped using PCR-RFLP method. The mRNA expression levels were measured using quantitative real time PCR. The maternal Dicer1 rs3742330 polymorphism was not associated with PE or PE severity; however, the placental Dicer1 rs3742330 AG genotype was associated with two fold higher risk of PE and three fold higher risk of severe PE (P = 0.018 and P = 0.005, respectively). The relative mRNA expression of Dicer1 gene in the placenta did not differ between the two groups. In addition, the relative mRNA expression of Dicer1 gene was significantly lower in the placenta of women with rs3742330 AG+GG genotypes in the total population (P = 0.028) and PE women (P = 0.004), but not in the control group. In conclusion, there was a relationship between placental but not maternal Dicer1 rs3742330 polymorphism and PE. There was no difference in Dicer1 mRNA expression between the PE and control groups; however, it was significantly lower in the placenta of women with rs3742330 AG+GG genotypes.

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Evidence has shown that pre-eclampsia (PE) is associated with an increased level of catecholamines. Renalase is a catecholamine-metabolizing enzyme, which contributes to the occurrence of hypertension. In the current study, we aimed to assess the relation between two renalase gene (RNLS) polymorphisms, including rs2576178 at the 5′-flanking region and rs10887800 at intron 6, near the exon/ intron border and PE susceptibility. In this case-control study, 179 women with PE and 202 normotensive pregnant women were genotyped for RNLS rs2576178 and rs10887800 polymorphisms by the polymerase chain reaction-restriction fragment length polymorphism method. There was no association between RNLS rs10887800 and rs2576178 polymorphisms and PE, neither in the dominant nor in the recessive model. Although there was no association between RNLS rs10887800 polymorphism and mild PE, this polymorphism was associated with 2.2-fold higher risk of severe PE in the recessive model (odds ratio [OR], 2.2; 95% confidence interval [CI], 1.2-4.4; P = 0.01) but not in the dominant model. The RNLS rs2576178 and rs10887800 polymorphisms were not associated with PE severity. The RNLS rs10887800 and rs2576178 GG/GG combined genotypes were associated with 8.4-and 16.7-fold higher risk of PE and severe PE, respectively (OR, 8.4; 95% CI, 1-71.1; P = 0.048 and OR, 16.7; 95% CI, 1.6-167; P = 0.018). Also, the G-G haplotype was associated with 1.7-fold risk of PE and mild PE (OR, 1.7; 95% CI, 1.1-2.4; P = 0.009 and OR, 1.7; 95% CI, 1.1-2.5; P = 0.02). The RNLS rs10887800 polymorphism was associated with severe PE. The RNLS rs10887800 and rs2576178 GG/GG combined genotypes and G-G haplotype were associated with higher risk of PE. K E Y W O R D S haplotype, Iran, polymorphism, renalase, severe pre-eclampsia (PE)

H19 is an imprinted gene transcribing a long noncoding RNA which was previously reported to be involved in some diseases. However, the association between the H19 polymorphisms and Pre-eclampsia (PE) susceptibility has remained elusive. This study aimed to evaluate the association between three H19 haplotype SNPs (rs3741219, rs217727, and rs2107425) and the risk of PE. The present case control study consisted of 193 PE women and 201 controls. The H19 rs3741219 and rs217727 polymorphisms were genotyped with PCR-RFLP (Polymerase chain reaction-restriction fragment length polymorphism) and the H19 rs2107425 polymorphism with ARMS-PCR (Amplification refractory mutation system) methods. The frequency of alleles and genotypes of H19 rs3741219 and rs2107425 polymorphisms did not differ between PE women and controls. The frequency of the H19 rs217727T allele was significantly higher in PE women (P < 0.0001). The H19 rs217727 polymorphism was associated with higher PE susceptibility in the Co-dominant (OR = 12.1, 95% CI = 5.7-24.5, P < 0.0001 for CT genotype and OR = 29.7, 95% CI = 12.9-68.1, P < 0.0001 for TT genotype), Dominant (OR = 15.1, 95% CI = 7.5-30.3, P = P < 0.0001), Recessive (OR = 4.5, 95% CI = 2.6-7.9, P = < 0.0001), and Over-dominant (OR = 2.1, 95% CI = 1.4-3.1, P = 0.0006) models. Furthermore, the CCC, TCT, TCC, and CCT haplotypes of H19 rs3741219, rs217727, rs2107425 were associated with lower risk of PE; however, the CTC, TTC, and TTT haplotypes were associated with higher risk of PE. In conclusion, the present study found the relationship between H19 rs217727 but not rs3741219 and rs2107425 polymorphisms and PE susceptibility. In addition, the CTC, TTC, and TTT haplotypes were associated with the higher risk of PE.

Preeclampsia (PE) is a pregnancy specific complication arises in presence of the placenta and disappears immediately after delivery. Therefore, the aim of the present study was to investigate the possible effects of the placental 3'-UTR rs1537514C>G and rs4846049C>A polymorphisms and DNA methylation of the MTHFR gene on the MTHFR mRNA expression. The placenta of 74 PE pregnant women and 75 normotensive pregnant women were collected after delivery. The methylation status of the MTHFR promoter was assessed with Methylation Specific PCR (MSP). The rs1537514C>G and rs4846049C>A polymorphisms were genotyped using PCR-RFLP method. The mRNA expression levels were measured by Quantitative Real Time PCR. The results showed the lower MTHFR mRNA expression in the placenta of PE women. There was an association between hypermethylation and lower MTHFR mRNA expression in PE women and entire women but not normotensive pregnant women. The frequency of MTHFR rs1537514CG genotype was significantly lower in PE women; however, there was no association between MTHFR rs4846049C>A polymorphism and PE. The combination effects of MTHFR CG/AC genotypes and G-A haplotype of MTHFR rs1537514/rs4846049 polymorphisms were associated with lower risk of PE. The MTHFR rs1537514G (4869G) allele was associated with higher MTHFR mRNA expression in both groups. However, there was no relation between MTHFR rs4846049C>A polymorphism and MTHFR mRNA expression. Our findings showed lower MTHFR mRNA expression in PE women. The MTHFR rs1537514C>G polymorphism was associated with lower PE risk and MTHFR mRNA expression. Lower expression of MTHFR mRNA was observed in the women with the hypermethylated promoter.

The Drosha rs10719TC and CC genotypes were associated with PE risk. The CC-GG combined genotype and C-G haplotype of Drosha rs10719 and rs6877842 polymorphisms may increase PE susceptibility.

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