Abstract
BackgroundReduced placental perfusion predisposes to the maternal syndrome pre-eclampsia characterized by systemically reduced perfusion. Considerable data support the role of angiogenic factors in the development of the maternal syndrome. Hypoxia-inducible factor (HIF-1) mediates the cellular responses to hypoxia e.g. by promoting angiogenesis.MethodsHere we studied whether two single nucleotide sequence variants, c.1744 C>T that changes residue 582 of HIF-1α from proline to serine (P582S) and c.1762 G>A that changes residue 588 of HIF-1α from alanine to threonine (A588T) in the exon 12 of the HIF1A gene, are associated with pre-eclampsia. We studied 108 women with pre-eclampsia in their first pregnancy, and 101 controls with normotensive pregnancies. Pre-eclampsia was defined as a blood pressure level of at least 140/90 mmHg in a woman who was normotensive before 20 weeks of gestation, and proteinuria at least of 0.3 g per 24-hour urine collection. The patients and controls were genotyped for variations in the exon 12 of HIF1A gene by sequencingResultsThe frequencies of the c.1744 C>T and c.1762G>A sequence variants were not significantly different between women with pre-eclamptic first pregnancies and women with normotensive pregnancies. In addition, two synonymous variants (c.1740G>A and c.1800A>T) were detected at comparable levels in the two groups. All variants were identified in the heterozygous form.ConclusionThe sequence variants in the exon 12 of the HIF1A gene were not associated with pre-eclampsia in the Finnish population.
Highlights
Reduced placental perfusion predisposes to the maternal syndrome pre-eclampsia characterized by systemically reduced perfusion
The sequence variants in the exon 12 of the HIF1A gene were not associated with pre-eclampsia in the Finnish population
All four SNP genotype frequencies in both patients and controls were in agreement with Hardy-Weinberg equilibrium (p > 0.05.)
Summary
Reduced placental perfusion predisposes to the maternal syndrome pre-eclampsia characterized by systemically reduced perfusion. Pre-eclampsia resolves after delivery, which is currently the only existing therapy. It is a heterogeneous disease, commonly mixed presentation of two categories: placental pre-eclampsia with origins primarily in abnormal placental perfusion and maternal pre-eclampsia with origins primarily in pre-existing problems in the mother [2]. Pre-eclampsia shares many common risk factors with atherosclerosis, such as pre-existing hypertension, diabetes, obesity, renal disease and the metabolic syndrome [3]. A large body of evidence suggests that pre-eclampsia is associated with increased risk of cardiovascular diseases in later life of both mother and baby [4,5]. Despite intensive research genetic factors predisposing pre-eclampsia are largely unknown [7,8]
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