RESUMEN
AIM: Fetal growth restriction (FGR) can lead to short-term and long-term impairments in the fetus. The placenta functions as an exchanger for substance transport, playing a critical role in fetal growth. However, the mechanism from the placental standpoint is still not fully understood. In this study, we aimed to investigate the pathophysiological mechanisms in the placenta that mediated the development of FGR and sex differences. METHODS: We analyzed the gene expression profiles of GSE100415 containing specific normotensive FGR placental samples and GSE114691 with canonical samples using three different methods, differentially expressed gene analysis, weighted gene co-expression network analysis, and gene set enrichment analysis. Gene enrichment was performed, including the gene ontology and pathway from the Kyoto Encyclopedia of Genes and Genomes. The important process was then validated in pregnant Wistar rats subcutaneously administered dexamethasone (0.2 mg/kg/d) or saline from gestation Day 9 to 21. RESULTS: Our results revealed little difference between the comparison of normal and normotensive FGR placental samples but confirmed the sex difference. Further analyses of the canonical samples identified the occurrence of vascular dysfunction, which was validated by the calculation of the vascular lumen area, showing that the vascular lumen in the FGR group was more than in the control. We also discovered 17 significantly expressed genes from the involved eigengenes. CONCLUSION: Our study provides an important theoretical and experimental basis to reevaluate the development of FGR from the placental standpoint and suggests a series of biomarkers for future clinical use.
