Elevated PGT promotes proliferation and inhibits cell apoptosis in preeclampsia by Erk signaling pathway

Prostaglandins participate in maternal recognition of pregnancy, implantation and maintenance of gestation. Prostaglandin transporter (PGT), as a candidate molecule of prostaglandin carriers, might be involved in the pathogenesis of preeclampsia. In preeclampsia (PE) patients' placental tissue, we identified PGT by RNA sequencing, measured its expression pattern by quantitative real-time PCR and Western blot. PGT was found to be upregulated in preeclamptic placental tissue. The expression pattern of PGT in PE was double confirmed by eight Gene Expression Omnibus (GEO) databases. In abortion tissues at 6-8 weeks, we then observed the cellular location of PGT by Immunofluorescence technique (IF) and found PGT located in trophoblast cell of the placenta of early pregnancy. In vitro studies revealed that forced expression of PGT in HTR8/Sveno cell inhibited its apoptosis, but promoted its proliferation by activating Erk signaling. In vivo study, we used reduced uterine perfusion pressure (RUPP) rat model and L-NAME-induced preeclampsia-like rats to study the possible role of PGT in preeclampsia. And PGT was found to be upregulated in both preeclampsia rat models by Immunohis-tochemical (IHC) staining. Newly identified PGT plays an important role in trophoblast proliferation via Erk signaling, providing new insights for understanding the pathogenesis of PE.

Automated summary

Prostaglandins are involved in maternal recognition of pregnancy, implantation, and maintenance of gestation. Prostaglandin transporter (PGT), a potential carrier molecule of prostaglandins, may play a role in the pathogenesis of preeclampsia. Through various techniques, PGT was found to be upregulated in preeclamptic placental tissue and its expression pattern was confirmed through multiple databases. Further studies showed that PGT is located in trophoblast cells of the placenta and its forced expression promotes trophoblast proliferation through the activation of the Erk signaling pathway. In animal models of preeclampsia, PGT was also found to be upregulated. These findings provide new insights into the understanding of the pathogenesis of preeclampsia.