Placenta accreta

Abstract

Article and journal characteristics
Introduction
Materials and methods
Results
Discussion
Conclusion
Questions for discussion
Outlines

Published in Archives of Gynecology and Obstetrics (Q2, h-index of 68, IF = 2.344, Open access journal) on 28 October 2020.
Original research.
Retrospective study.
20 female patients were devided into 2 groups based on their placental status (n=10 of placenta accreta; n=10 normal control placentas).
Tissue samples were collected from January 2015 through April 2019.
References: 44 articles
Article and journal characteristics

Placenta accreta, and its most severe demonstration placenta percreta, invades through all the uterine layers and is considered a dangerous condition that may lead to a life threatening bleeding after the delivery.
The most shared theory of placenta accreta pathogenesis is that defective decidualization involving the endometrial–myometrial interface, such as in areas of scarring caused by previous uterine surgery, allows the anchoring villi of the placenta to attach directly to or invade the myometrium.
Prior cesarean delivery (CD) and placenta previa are independent risk factors for placenta accrete.
Introduction

The two major cells in the placenta include villous trophoblasts (VT) and extravillous trophoblast (EVT). VT cells cover the chorionic villi and are involved in the exchange of gas and nutrients between the mother and the fetus, while EVT cells, which migrate and invade into the maternal endometrium, are one of the central components of human implantation and placentation.
αvβ3 integrin is a heterodimeric transmembrane glycoprotein that facilitate cell–ECM adhesion, cell migration, signal transduction and cell to cell interaction.
Introduction

Materials and methods

Baseline characteristics of the study group.
Materials and methods

Total protein extraction from all placental tissues and following αvβ3 integrin expression assessment by WB using an anti β3 integrin monomer antibody showed significantly elevated αvβ3 protein levels in the percreta tissues compared to normal placentas (p<0.05).
Representative WB results from four normal and four percreta placentas are depicted in the figure.
Actin was used as a loading control marker.
Results

Normalized quantification of the integrin level in the entire study cohort is shown in the figure.
Significantly elevated αvβ3 protein levels in the percreta tissues compared to normal placentas (p<0.05).
Results

Results

Results
Results of αvβ3 IHC staining in EVT cells in all collected placentas indicate that in the majority of percreta placentas (9 out of 10 tissues), EVT cells consistently exhibited signifcantly elevated αvβ3 integrin compared to the expression level in normal placentas.
In the EVT cells the expression of αvβ3 was uniformly distributed.

Results
In contrast, VT cells in the normal and percreta placentas demonstrates a comparable integrin expression (7 out of 10 tissues).
In the VT cells the integrin was located mostly at the cell membrane, with an apical expression.

We identified enhanced αvβ3 integrin expression in placenta percreta, compared to normal placentas, which mainly originated from EVT cells.
We observed a membrane expression in VT cells and a uniformly diffused expression in EVT cells.
We suggest that placenta percreta utilizes this specific integrin to display abnormal invasive phenotype.
Discussion

To study the integrin localization we used an antibody that recognizes the full αvβ3 integrin dimeric form, and not the integrin monomers, as commonly used by others.
Additional strength is provided by previous works on the integrin in EVT cells, which support their involvement in placenta accreta.
Possible limitations are the small study size and its descriptive nature.
Discussion

αvβ3 integrin is overexpressed in placenta percreta tissues, originating mainly from EVT cells, and suggest for a potential function of this membrane receptor in the pathogenesis of this condition.
Due to rarity of this condition, additional studies are needed to validate these findings in a larger study cohort. In addition, more work is merited in order to fully elucidate the biological role of αvβ3 integrin using in vitro and in vivo models.
Conclusion

What are the potential benefits of using knowledge of αvβ3 integrin overexpression in treatment and diagnosis of placenta accreta?
Does the discovery of αvβ3 integrin overexpression in EVT cells in placenta percreta significantly improves the understanding of the pathogenesis of placenta accreta?
What are the new perspectives and potential targets in studying the pathogenesis of placenta accreta?
Questions for discussion