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Common variants of fetal and maternal complement genes in preeclampsia: pregnancy specific complotype

Manu Banadakoppa1, Meena Balakrishnan2, Chandra Yallampalli3

  • 1Department of Obstetrics & Gynecology, Baylor College of Medicine, Houston, Texas, USA. banadako@bcm.edu.

Scientific Reports
|March 18, 2020
PubMed

Insights

Preeclampsia (PE) risk may be linked to specific genetic variations in maternal and fetal complement genes, forming unique "complotypes." These genetic combinations appear more common in women with PE, suggesting a predisposition.

Area of Science:

  • Immunogenetics
  • Reproductive Medicine
  • Perinatal Health

Background:

  • Preeclampsia (PE) is a pregnancy-specific hypertensive disorder with potential life-threatening complications like eclampsia.
  • Elevated systemic complement activation and placental deposition are observed in PE pregnancies.
  • The role of genetic variations in complement pathways predisposing to PE requires further investigation.

Purpose of the Study:

  • To investigate the hypothesis that combinations of common single nucleotide polymorphisms (SNPs) in maternal and fetal complement genes form pregnancy-specific complotypes that predispose women to PE.
  • To identify common SNPs in maternal (factor H, C3) and fetal (CD46) complement genes and analyze their association with PE.
  • To examine the relationship between identified genetic variants, placental complement deposition, and maternal alternative pathway activity.

Main Methods:

  • Sequencing of maternal factor H (CFH) and C3 genes, and fetal CD46 gene to identify common SNPs.
  • Genotyping analysis to determine the prevalence of identified SNPs and complotypes in PE patients and normotensive controls.
  • Measurement of placental complement deposition and maternal alternative pathway 50 (AP50) activity.
  • Assessment of placental CD46 expression and association with specific CD46 variants.

Main Results:

  • Nine common SNPs were identified in the studied complement genes.
  • Two fetal CD46 SNPs showed significantly higher minor allele frequencies in PE patients.
  • Complotypes combining fetal CD46 variants with maternal CFH/C3 variants were more prevalent in PE pregnancies.
  • Higher placental complement deposition and maternal AP50 values were observed in PE pregnancies.
  • Specific CD46 variants correlated with reduced placental CD46 expression, and a CFH variant with increased maternal AP50.

Conclusions:

  • Specific combinations of maternal and fetal complement gene variants (complotypes) are associated with an increased prevalence in preeclampsia.
  • Fetal CD46 and maternal CFH/C3 gene variants may play a role in PE susceptibility.
  • Genetic variations in complement genes influence placental complement deposition and maternal alternative pathway activity, contributing to PE pathophysiology.

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