FABP4 Downregulated by FOS Alleviates Palmitic Acid-induced Endothelial Cell Dysfunction Via Inactivating ERK/STAT-1 Signaling Pathway

This study aimed to explore the role and the mechanism of FABP4 in the pathogenesis of preeclampsia (PE). FABP4 expression in the whole blood and the placental tissue of PE patients and healthy pregnant women was detected using RT-qPCR. The transfection efficacy of sh-FABP4, sh-FOS and Ov-FOS was examined using Western blotting and RT-qPCR. CCK-8 assay was used to detect cell viability. TUNEL assay was used to detect cell apoptotic level. Wound healing and transwell assays were used to detect the migration and invasion of HUVECs. Tube formation assay was used to detect HUVEC s’ angiogenic ability. Western blotting was used to measure the expressions of apoptosis- and ERK/STAT-1 signaling pathway-related proteins. Luciferase reporter assay was used to detect FABP4 promoter activity, while ChIP assay confirmed the binding ability of FOS to FABP4. FABP4 expression was increased in the whole blood and the placental tissue of PE patients and palmitic acid (PA)-treated HUVECs. FABP4 interference inhibited apoptosis while promoting the migration, invasion, and angiogenesis in PA-induced HUVECs via inactivating ERK/STAT-1. It was also identified that FOS reduced FABP4 activity and inhibited FABP4/ERK/STAT-1 signaling pathway. FABP4 protected against PA-induced endothelial cell dysfunction via the inhibition of ERK/STAT-1, which might be mediated by FOS.