Common and recurrent dysregulated molecular network of placental hypoxia and associated vasculogenesis and angiogenesis in fetal growth restriction
Wei Li, Xiaoyi Bai, Oi Ka Chan, Maran Bo Wah Leung, So Ling Lau, Chi Chiu Wang, Tak Yeung Leung
TL;DR
This study identifies a molecular network involving hypoxia and blood vessel formation in placental dysfunction linked to fetal growth restriction.
Contribution
The study reveals a novel dysregulated molecular network involving HIF1A and VEGFA in placental hypoxia and angiogenesis in fetal growth restriction.
Findings
69 differentially expressed mRNAs and eight miRNAs were identified in FGR/sFGR placentae.
HIF1A and VEGFA were key nodes in the molecular network related to hypoxia and angiogenesis.
Upregulated HIF1A and VEGFA expression was validated and associated with clinical severity in sFGR twins.
Abstract
Fetuses with fetal growth restriction (FGR) and selective FGR (sFGR) face elevated health risks both before and after birth. Although the underlying pathomechanisms remain unclear, placental dysfunction is recognized as a major contributing factor. By integrating untargeted transcriptomic data from FGR/sFGR placentae, this study identified 69 differentially expressed mRNAs (DEmRs) and eight differentially expressed miRNAs (DEmiRs). Functional enrichment analysis demonstrated significant enrichment in the angiogenesis and vasculogenesis pathways, with the hypoxia-related genes HIF1A and VEGFA serving as key nodes in the molecular network. Further validation through RNA sequencing (RNAseq), quantitative real-time PCR (RT-qPCR), and immunohistochemistry demonstrated that the expression of the transcriptional regulator HIF1A and the angiogenic factor VEGFA was upregulated in the placentae…
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Taxonomy
TopicsPregnancy and preeclampsia studies · Birth, Development, and Health · Neonatal and fetal brain pathology