Maternal angiotensinogen (AGT) haplotypes, fetal renin (REN) haplotypes and risk of preeclampsia; estimation of gene-gene interaction from family triad data
Preeclampsia is a debilitating disorder affecting approximately 3% of pregnant women in the Western world. Although inconclusive, current evidence suggests that the renin-angiotensin system may be involved in hypertension.
Therefore, our objective was to determine whether the genes for placental renin (REN) and maternal angiotensinogen (AGT) interact to influence the risk of preeclampsia.
Methods: Three haplotype-tagging SNPs (htSNPs) covering REN (rs5705, rs1464818, and rs3795575) and another three covering AGT (rs2148582, rs2478545, rs943580) were genotyped in 99 mother-father-child triads of preeclampsia pregnancies. We estimated relative risks (RR) conferred by maternal AGT and fetal REN haplotypes using HAPLIN, a statistical software designed to detect multi-marker transmission distortion among triads.
To assess for a combined effect of maternal AGT and fetal REN haplotypes, the preeclamptic triads were stratified according to the presence or absence of maternal AGT haplotype C-T-A and tested for an effect of fetal REN across these strata.
Results: We found evidence that mothers carrying the most frequent AGT haplotype, C-T-A, had a reduced risk of preeclampsia (RR of 0.4, 95% CI = 0.2-0.8 for heterozygotes and 0.6, 95% CI = 0.2-1.5 for homozygotes). Risk estimates for maternal homozygous carriers of AGT haplotypes t-c-g and C-c-g appeared to be higher, with only the former being statistically significant.
We found no evidence of an overall effect of fetal REN haplotypes and no support for our hypothesis that an effect of REN depended on whether the mother carried the C-T-A haplotype of AGT (p = 0.33).
Conclusion: Our findings indicate that the mother's AGT haplotypes affect her risk for developing preeclampsia. However, this risk was not influenced by REN haplotypes.
Author: Hege VefringLine WeeAstanand JugessurHakon GjessingStein NilsenRolv Lie
Credits/Source: BMC Medical Genetics 2010, 11:90
Published on: 2010-06-10
Copyright by the authors listed above - made available via BioMedCentral (Open Access). Please
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