THBS1 regulates trophoblast fusion through a CD36-dependent inhibition of cAMP, and its upregulation participates in preeclampsia

Bibliographic Details
Title: THBS1 regulates trophoblast fusion through a CD36-dependent inhibition of cAMP, and its upregulation participates in preeclampsia
Authors: Fu-Mei Duan, Li-Juan Fu, Yong-Heng Wang, Enoch Appiah Adu-Gyamfi, Ling- Ling Ruan, Zeng-Wei Xu, Shi-Quan Xiao, Xue-Mei Chen, Ying-Xiong Wang, Tai-Hang Liu, Yu-Bin Ding
Source: Genes and Diseases, Vol 8, Iss 3, Pp 353-363 (2021)
Publisher Information: KeAi Communications Co., Ltd., 2021.
Publication Year: 2021
Collection: LCC:Medicine (General)
LCC:Genetics
Subject Terms: cAMP, Cell fusion, Preeclampsia, THBS1, Trophoblast, Medicine (General), R5-920, Genetics, QH426-470
More Details: Preeclampsia is a pregnancy complication which threatens the survival of mothers and fetuses. It originates from abnormal placentation, especially insufficient fusion of the cytotrophoblast cells to form the syncytiotrophoblast. In this study, we found that THBS1, a matricellular protein that mediates cell-to-cell and cell-to-matrix interactions, is downregulated during the fusion of primary cytotrophoblast and BeWo cells, but upregulated in the placenta of pregnancies complicated by preeclampsia. Also, THBS1 was observed to interact with CD36, a membrane signal receptor and activator of the cAMP signaling pathway, to regulate the fusion of cytotrophoblast cells. Overexpression of THBS1 inhibited the cAMP signaling pathway and reduced the BeWo cells fusion ratio, while the effects of THBS1 were abolished by a CD36-blocking antibody. Our results suggest that THBS1 signals through a CD36-mediated cAMP pathway to regulate syncytialization of the cytotrophoblast cells, and that its upregulation impairs placental formation to cause preeclampsia. Thus, THBS1 can serve as a therapeutic target regarding the mitigation of abnormal syncytialization and preeclampsia.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2352-3042
Relation: http://www.sciencedirect.com/science/article/pii/S2352304220300726; https://doaj.org/toc/2352-3042
DOI: 10.1016/j.gendis.2020.05.007
Access URL: https://doaj.org/article/5a166452b85945d7ba6b5d35f787c077
Accession Number: edsdoj.5a166452b85945d7ba6b5d35f787c077
Database: Directory of Open Access Journals
More Details
ISSN:23523042
DOI:10.1016/j.gendis.2020.05.007
Published in:Genes and Diseases
Language:English