Prenatal diagnosis · 2025
mRNA Expression to Assess Hypoxia and Angiogenesis in Decidual Tissue of Term Fetuses With a Congenital Heart Disease.
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Snoep Maartje C, van der Hoorn Marie-Louise P, Aliasi Moska, Anholts Jacqueline D H, Ruiter Marco C De, van der Meeren Lotte E, Eikmans Michael, Haak Monique C
Аннотация
OBJECTIVE: Delayed fetal neurodevelopment, lower birth weight, and placental abnormalities are related to congenital heart defects (CHD). We explored mRNA expression assessment of candidate genes related to fetal hypoxia and angiogenesis in decidual tissues of pregnancies with different types of fetal CHD, classified based on aortic flow and oxygenation.
METHOD: In this prospective case-control study, mRNA expression was assessed for 18 candidate genes related to fetal hypoxia and angiogenesis in decidual (maternal) tissues of fetal simple transposition of the great arteries (TGA) (n = 14) and left sided CHD (n = 13) and in healthy controls (n = 31). Cases with a fetal syndrome/genetic abnormality, termination of pregnancy, intra-uterine fetal demise, or multiple pregnancies were excluded.
RESULTS: There were no significant differences in gene expression of the candidate genes between CHD cases and controls and between cases with fetal simple TGA and cases with fetal left sided CHD. Clustering analysis did not differentiate subgroups within the study population.
CONCLUSIONS: Fetal hypoxia and altered angiogenesis on the level of mRNA expression in decidual tissue were not significantly different between CHD cases and controls and between cases with fetal simple TGA and cases with fetal left sided CHD. We hypothesize that other (angio) genetic and molecular pathways lead to morphological placental alterations in pregnancies with fetal CHD.
METHOD: In this prospective case-control study, mRNA expression was assessed for 18 candidate genes related to fetal hypoxia and angiogenesis in decidual (maternal) tissues of fetal simple transposition of the great arteries (TGA) (n = 14) and left sided CHD (n = 13) and in healthy controls (n = 31). Cases with a fetal syndrome/genetic abnormality, termination of pregnancy, intra-uterine fetal demise, or multiple pregnancies were excluded.
RESULTS: There were no significant differences in gene expression of the candidate genes between CHD cases and controls and between cases with fetal simple TGA and cases with fetal left sided CHD. Clustering analysis did not differentiate subgroups within the study population.
CONCLUSIONS: Fetal hypoxia and altered angiogenesis on the level of mRNA expression in decidual tissue were not significantly different between CHD cases and controls and between cases with fetal simple TGA and cases with fetal left sided CHD. We hypothesize that other (angio) genetic and molecular pathways lead to morphological placental alterations in pregnancies with fetal CHD.