TLR9 (Toll-Like Receptor 9) Agonist Suppresses Angiogenesis by Differentially Regulating VEGFA (Vascular Endothelial Growth Factor A) and sFLT1 (Soluble Vascular Endothelial Growth Factor Receptor 1) in Preeclampsia

Author:

He Biwei1,Yang Xingyu1,Li Yamei1,Huang Ding1,Xu Xin1,Yang Wenjun1,Dai Yan1,Zhang Huijuan1,Chen Zhengjun1,Cheng Weiwei1

Affiliation:

1. From the International Peace Maternity and Child Health Hospital (B.H., X.Y., Y.L., D.H., W.Y., H.Z., W.C.), Institute of Embryo-Fetal Original Adult Disease (X.Y.), and Department of Obstetrics and Gynecology, Xinhua Hospital (X.X.), School of Medicine, Shanghai Jiao Tong University, China; State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Science (Y.D., Z.C.); and School of Life Science and...

Abstract

Preeclampsia is a common pregnancy-specific disorder characterized by elevated blood pressure and proteinuria. Activation of the maternal immune system and impaired placental angiogenesis are thought to contribute to the pathogenesis of preeclampsia. TLR9 (Toll-like receptor 9) plays a role in innate immunity, defending the organism against infection. The purpose of this study was to determine whether TLR9 inhibits angiogenesis at the fetomaternal interface under conditions of preeclampsia. We confirmed the downregulation of VEGFA (vascular endothelial growth factor A) and upregulation of TLR9 and sFLT1 (soluble vascular endothelial growth factor receptor 1) in placentas from preeclamptic women. Then, we established a mouse model with preeclampsia-like symptoms using the synthetic TLR9 agonist CpG (cytidine–phosphate–guanosine)-ODN (oligodeoxynucleotide; ODN1826). We observed the downregulation of VEGFA and the upregulation of sFLT1 in placentas from the preeclampsia-like animal model and in trophoblasts treated with CpG-ODN (ODN2006). In addition, silencing TLR9 promoted the migration and invasion of HTR8/SVneo cells. In conclusion, TLR9 is capable of robustly suppressing angiogenesis by differentially regulating the expression of VEGFA and sFLT1 at the fetomaternal interface, potentially contributing to the development of preeclampsia.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

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