In summary, we successfully established a new rat model of preeclampsia by single administration of ultra-low-dose LPS upon placentation, in which the activation of placental TLR4 signaling in response to LPS elicited deficient trophoblast invasion and SA remodeling contributing to poor placentation that may reach maximum intensities in the preeclampsia-like syndrome. This evidence concerns the gene TLR4 and preeclampsia.