» Articles » PMID: 27468655

Trophoblastic Debris Modifies Endothelial Cell Transcriptome in Vitro: a Mechanism by Which Fetal Cells Might Control Maternal Responses to Pregnancy

Overview
Journal Sci Rep
Specialty Science
Date 2016 Jul 30
PMID 27468655
Citations 12
Authors
Affiliations
Soon will be listed here.
Abstract

The mechanisms by which the fetus induces maternal physiological adaptations to pregnancy are unclear. Cellular debris, shed from the placental syncytiotrophoblast into the maternal blood and phagocytosed by maternal endothelial and immune cells, may be one of these mechanisms. Here we show that trophoblastic debris from normal first trimester placentae induces changes in the transcriptome and proteome of endothelial cells in vitro, which might contribute to the adaptation of the maternal cardiovascular system to pregnancy. Trophoblastic debris also induced endothelial cells to transcribe placenta-specific genes, including the vasodilator hormone CSH1, thereby expanding the effective functional size of the placenta. Our data suggest that the deportation of trophoblastic debris is an important part of the complex network of feto-maternal communication.

Citing Articles

Disruption of maternal vascular remodeling by a fetal endoretrovirus-derived gene in preeclampsia.

Gong X, He W, Jin W, Ma H, Wang G, Li J Genome Biol. 2024; 25(1):117.

PMID: 38715110 PMC: 11075363. DOI: 10.1186/s13059-024-03265-z.


Placenta: an old organ with new functions.

Khorami-Sarvestani S, Vanaki N, Shojaeian S, Zarnani K, Stensballe A, Jeddi-Tehrani M Front Immunol. 2024; 15:1385762.

PMID: 38707901 PMC: 11066266. DOI: 10.3389/fimmu.2024.1385762.


A pilot in vivo study: potential ovarian cancer therapeutic by placental extracellular vesicles.

Chen X, Tijono S, Tsai B, Chamley L, Ching L, Chen Q Biosci Rep. 2023; 43(8).

PMID: 37503762 PMC: 10442519. DOI: 10.1042/BSR20230307.


Modelling human placental villous development: designing cultures that reflect anatomy.

James J, Lissaman A, Nursalim Y, Chamley L Cell Mol Life Sci. 2022; 79(7):384.

PMID: 35753002 PMC: 9234034. DOI: 10.1007/s00018-022-04407-x.


Effects of anti-beta 2-glycoprotein 1 antibodies and its association with pregnancy-related morbidity in antiphospholipid syndrome.

Fierro J, Velasquez M, Cadavid A, de Leeuw K Am J Reprod Immunol. 2021; 87(1):e13509.

PMID: 34738282 PMC: 9285810. DOI: 10.1111/aji.13509.


References
1.
Germain S, Sacks G, Sooranna S, Soorana S, Sargent I, Redman C . Systemic inflammatory priming in normal pregnancy and preeclampsia: the role of circulating syncytiotrophoblast microparticles. J Immunol. 2007; 178(9):5949-56. DOI: 10.4049/jimmunol.178.9.5949. View

2.
Tong M, Chamley L . Placental extracellular vesicles and feto-maternal communication. Cold Spring Harb Perspect Med. 2015; 5(3):a023028. PMC: 4355256. DOI: 10.1101/cshperspect.a023028. View

3.
Park H, Kwon H, Lim H, Hong B, Lee J, Park B . Potential role of leptin in angiogenesis: leptin induces endothelial cell proliferation and expression of matrix metalloproteinases in vivo and in vitro. Exp Mol Med. 2001; 33(2):95-102. DOI: 10.1038/emm.2001.17. View

4.
Wei J, Chen Q, James J, Stone P, Chamley L . IL-1 beta but not the NALP3 inflammasome is an important determinant of endothelial cell responses to necrotic/dangerous trophoblastic debris. Placenta. 2015; 36(12):1385-92. DOI: 10.1016/j.placenta.2015.10.011. View

5.
Askelund K, Chamley L . Trophoblast deportation part I: review of the evidence demonstrating trophoblast shedding and deportation during human pregnancy. Placenta. 2011; 32(10):716-23. DOI: 10.1016/j.placenta.2011.07.081. View