IGF1 is Reduced in Pregnancies with Preeclampsia and its Influence on Biological Behavior of Trophoblast Cells

Preeclampsia (PE) is a serious pregnancy complication characterized by impaired trophoblast function. Insulin-like growth factor-1 (IGF1) is a peptide hormone that exhibits metabolic effects similar to insulin, modulating diverse physiological processes such as cellular proliferation, differentiation, motility, survival, and gene expression regulation. The objective of this study was to investigate the expression level and biological function of IGF1 in PE. The expression level of the IGF1 was quantified by quantitative real-time polymerase chain reaction (RT-qPCR). Functional phenotypes in IGF1-regulated HTR8/SVneo cells were assessed; cell proliferation, migration, invasion, cell cycle, and apoptosis were determined by CCK8 assays, wound healing assays, Transwell assays, and flow cytometry, respectively. Compared to normal pregnancy, preeclamptic placental tissues exhibited significantly downregulated IGF1 expression levels. Functional analyses revealed that IGF1 knockdown suppressed proliferation, migration, and invasion in HTR-8/SVneo cells, whereas IGF1 upregulation enhanced these functions. Both IGF1 knockdown and overexpression were performed without influencing the cell cycle or inducing apoptosis. These findings indicate that IGF1 serves as a critical mediator of trophoblast proliferation, migration, and invasion, contributing to preeclampsia development, providing novel insights of PE pathogenesis.