MBL Interferes with Endovascular Trophoblast Invasion in Pre-Eclampsia

Chiara Agostinis,Elisa Masat,Francesco De Seta,Fleur Bossi,Francesco Tedesco,Roberta Bulla,Maddalena Tonon,Oriano Radillo

doi:10.1155/2012/484321

Abstract

The spiral arteries undergo physiologic changes during pregnancy, and the failure of this process may lead to a spectrum of pregnancy disorders, including pre-eclampsia. Our recent data indicate that decidual endothelial cells (DECs), covering the inner side of the spiral arteries, acquire the ability to synthesize C1q, which acts as a link between endovascular trophoblast and DECs favouring the process of vascular remodelling. In this study, we have shown that sera obtained from pre-eclamptic patients strongly inhibit the interaction between extravillous trophoblast (EVT) and DECs, preventing endovascular invasion of trophoblast cells. We further demonstrated that mannose-binding lectin (MBL), one of the factor increased in pre-eclamptic patient sera, strongly inhibits the interaction of EVT with C1q interfering with the process of EVT adhesion to and migration through DECs. These data suggest that the increased level of MBL in pre-eclampsia may contribute to the failure of the endovascular invasion of trophoblast cells.

Highlights

The decidua is a newly formed tissue on the maternal side of human placenta and is characterized by active angiogenesis and structural modifications of the spiral arteries in the early phase of pregnancy
We further demonstrated that mannose-binding lectin (MBL), one of the factor increased in pre-eclamptic patient sera, strongly inhibits the interaction of extravillous trophoblast (EVT) with C1q interfering with the process of EVT adhesion to and migration through decidual endothelial cells (DECs)
We have shown that sera obtained from PE patients strongly inhibit the interaction between EVT and DECs, thereby controlling endovascular invasion of trophoblast cells, a fundamental process for the progression of pregnancy

Summary

Introduction

The decidua is a newly formed tissue on the maternal side of human placenta and is characterized by active angiogenesis and structural modifications of the spiral arteries in the early phase of pregnancy These changes, that include gradual loss of the musculoelastic structure of the arterial wall and replacement by amorphous fibrinoid material, are essential to create vessels of low resistance unresponsive to vasoconstrictive agents [1, 2] allowing continuous blood flow in the intervillous space. We have provided data indicating that decidual endothelial cells (DECs) lining the spiral arteries acquire the ability to synthesize C1q This protein binds avidly to the cell surface and acts as a physical link between endovascular trophoblast and DECs favouring the process of vascular remodelling [4]. The system is involved in the elimination of dead or modified self cells [6], but new roles in inflammatory, immunological processes, and tissue remodelling are emerging

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