Abstract
The abnormal production of matrix metalloproteinases (MMPs), especially MMP-9 and MMP-2, plays a pivotal role in hypertensive disorders of pregnancy, and as such, can influence the development of preeclampsia. These alterations may result from functional genetic polymorphisms in the promoter region of MMP-9 and MMP-2 genes, which modify MMP-9 and MMP-2 expression. We investigated the association of MMP-9 polymorphism rs3918242 (-1562 C>T) and MMP-2 polymorphism rs2285053 (-735 C>T) with the risk of preeclampsia. This case–control study was conducted on 345 women with preeclampsia and 281 age-matched women with normal pregnancies from Tunisian hospitals. Genomic DNA was extracted from whole blood collected at delivery. Genotypes for -1562 C>T and -735 C>T polymorphisms were performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). An increased frequency of heterozygous MMP-9 -1562 C/T genotype carriers was observed in women with preeclampsia compared to healthy controls (p = 0.03). In contrast, the MMP-2 -735 C>T polymorphism was not significantly different regarding frequency distribution of the allele and genotype between healthy pregnant women and women with preeclampsia. Our study suggests that the MMP-9 -1562 C/T variant, associated with high MMP-9 production, could be a genetic risk factor for preeclampsia in Tunisian women.
Highlights
As genetic variations may differ, depending on ethnicity [35,36], the present study aimed to evaluate the association of matrix metalloproteinases (MMPs)-2 -735 C>T and MMP-9 -1562 C>T polymorphisms with the risk of PE in a large Tunisian cohort
Our results showed a lack of association between the tested MMP-9 and MMP-2 polymorphisms and the severity of PE, irrespective of the genetic model used (Table 4)
MMP-9 promoter polymorphism could influence the risk of PE development through increased production of MMP-9 protein in the maternal circulation and at the maternal–fetal interface
Summary
Preeclampsia (PE) is a multi-system pregnancy-specific disorder classically characterized by elevated maternal blood pressure and proteinuria after 20 weeks of pregnancy. This syndrome complicates 5–7% of pregnancies worldwide and is responsible for. 60,000 maternal deaths annually, and a far greater number of fetal and neonatal deaths [1]. It is one of the leading causes of maternal and fetal mortality and morbidity [2,3]. PE has been proposed to result from multiple factors, such as angiogenic, inflammatory, and immune response, potentially due to genetic and external environmental 4.0/). The role of genetic predisposition is still not well understood, there is clear evidence of the contribution of family history supported by several segregation and linkage analysis studies, as well as genome-wide association studies [5]
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