Therapeutic potential of omentin-1 in preeclampsia: enhancing fetal outcomes, vascular function, and reducing inflammation

Abstract

This study evaluated the therapeutic potential of omentin-1 in preeclampsia (PE), focusing on fetal outcomes, vascular function, and inflammation. A PE-like mouse model received recombinant human omentin-1 protein (rh-omentin) from gestation day (gd) 13.5 to 16.5. On gd 17.5, fetuses and placentas were weighed, and serum sFlt-1 levels were measured. Maternal aortic rings were used for ex vivo vascular reactivity assays. Inflammatory factors and KLF2 expression in placental and aortic tissues were assessed using qPCR. HUVECs were exposed to plasma from PE patients or healthy pregnant individuals to evaluate omentin-1 and KLF2 expression by qPCR, with additional evaluation of KLF2 after rh-omentin treatment. Rh-omentin treatment reduced blood pressure in the PE-like model, accompanying by increased fetal and placental weights and higher fetal/placental weight ratios compared to untreated PE mice. Additionally, rh-omentin enhanced endothelial function in maternal aortic rings, as well as reduced placental necrosis and promoted CD31-positive vasculature in the labyrinth zone. Moreover, rh-omentin decreased pro-inflammatory factors (Il-1β, Il-6, and Tnf-α) in aortic and placental tissues of PE mice. KLF2 expression was restored in both aortic and placental tissues of PE mice and in HUVECs exposed to PE plasma following rh-omentin treatment. Rh-omentin improved fetal and placental outcomes in PE-like mice, enhancing vascular function and reducing inflammation in aortic and placental tissues. It also restored KLF2 expression in PE tissues and HUVECs exposed to PE plasma, suggesting therapeutic potential for addressing endothelial dysfunction in PE.