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Implantation and Pregnancy

Session: Poster Session A

(158) Maternal Circulating CD31+ Exosomes from Placental Accreta Stimulate Human Trophoblast Migration and Invasion

Wednesday, July 30, 2025
8:30 AM - 9:30 AM EDT
Location: Marquis Ballroom 6-10
Abstract Authors:

Alejandra Garcia Salmeron1; Olamide Tolulope Fategbe1; Qianrong Qi1; Joshua Makhoul1; Zhifen Yang1; Devesh Naidoo1; Carol Major2; Ruofan Yao2; Dong-bao Chen1

1. Department of Obstetrics & Gynecology, University of California, Irvine, CA 92697

2. Department of Obstetrics & Gynecology, Loma Linda University, CA 92350



Abstract Text:



Introduction: Trophoblast invasion is a critical phase of early placentation. Dysfunctional invasion can lead to serious pregnancy complications. In the case of placenta accreta spectrum (PAS), dysregulation leads to deep invasion of the myometrium, whereas preeclampsia is hallmarked with trophoblast under-invasion. Although the exact pathogenesis of PAS is currently unknown, we posited the active substances secreted from PAS lesions may circulate into maternal bloodstream where it can be identified. Trophoblast invasion is the major histopathologic phenotypes in PAS, herein we tested a hypothesis that maternal circulating CD31+ endothelial cell-derived exosomes in PAS patients stimulate trophoblast differentiation and invasion.



Methods: Blood samples were collected prior to cesarean delivery from pregnant persons who were normotensive, had preeclampsia with severe features, and antenatally diagnosed PAS pregnant ( >33 weeks’ gestation, n=10/group). Serum was separated and used to isolate total exosomes. Cell-specific exosomes of endothelial and trophoblast origins were purified by cell sorting respectively with anti-CD31 or anti-placenta alkaline phosphatase (PLAP) antibody-conjugated magnetic beads. Purified exosomes were transfected into human trophoblast stem cells (hTSC) and a trophoblast HTR8 cell line. All cultures were with medium containing 10% exosome-free fetal bovine serum. Differentiation of hTSC was accessed by markers of syncytiotrophoblasts and extravillous trophoblasts.  Morphological changes and hCG secretion were also measured. Matrigel-coated trans-wells were used to determine trophoblast migration and invasion.



Results: Compared to normal and preeclampsia, CD31+ exosomes were greater in maternal sera from patients with PAS, while PLAP+ exosomes were greater in maternal sera in patients with preeclampsia. PAS sera significantly stimulated HTR8 cell migration and invasion; these effects were abolished by removal of CD31+ but not PALP+ exosomes using antibody coated beads. Transfection of purified CD31+ (not PALP+) exosomes from PAS sera stimulated HTR8 cell migration and invasion. Incubation with CD31+ (not PALP+) exosomes stimulated migration and invasion of extravillous trophoblasts differentiated from hTSC.



Conclusion: Maternal circulating CD31+ exosomes from pregnant women with PAS stimulate trophoblast differentiation and invasion (Supported by NIH grants).