Abstract
The syncytiotrophoblast (STB) is a multinuclear layer forming the outer surface of the fetal part of the placenta deriving from villous cytotrophoblastic cell (vCTB) fusion and differentiation. This syncytialization process is characterized by morphological and biochemical alterations of the trophoblast, which probably require removal of pre-existing structures and proteins to maintain cell homeostasis and survival. Interestingly, autophagy, which allows degradation and recycling of cellular components, was shown to be activated in syncytiotrophoblast. Here we examined the involvement of endoplasmic reticulum stress (ERS) response in autophagy activation during vCTB syncytialization. We first demonstrated the activation of ERS response and autophagy during the time course of trophoblastic cell fusion and differentiation. Alteration of autophagy activation in vCTB by chemical treatments or Beclin-1 expression modulation leads to a decrease in trophoblastic syncytialization. Furthermore, ERS response inhibition by chemical treatment or siRNA strategy leads to a default in syncytialization, associated with alteration of autophagy markers and cell survival. From these data, we suggest that ERS response, by fine regulation of autophagy activation, may serve as an adaptive mechanism to promote cell survival during trophoblastic syncytialization.
Highlights
The placenta is a highly specialized transient organ that protects, oxygenizes, and nourishes the developing fetus by linking maternal and fetal circulation[1]
The mature chorionic villi are covered by an essential multinucleated continuous monolayer, the syncytiotrophoblast (STB), which is in direct contact with the maternal blood and functions as a nutrients and gas carrier, hormone secretion organ (β-human chorionic gonadotropin (β-hCG), steroids, Correspondence: Marie Cohen 1Department of Pediatrics, Gynecology and Obstetrics, Faculty of Medicine, University of Geneva, 1206 Geneva, Switzerland Edited by G.M
We have demonstrated that UPR and autophagy are directly implicated in villous cytotrophoblastic cell (vCTB) cell fusion and differentiation
Summary
The placenta is a highly specialized transient organ that protects, oxygenizes, and nourishes the developing fetus by linking maternal and fetal circulation[1]. Vascularized structures, referred to as chorionic villi, are involved in the efficient exchange of different molecules necessary for fetal development[2]. The formation of these complex multilayered structures is orchestrated by cytotrophoblastic cells (CTB)[3]. The mature chorionic villi are covered by an essential multinucleated continuous monolayer, the syncytiotrophoblast (STB), which is in direct contact with the maternal blood and functions as a nutrients and gas carrier, hormone secretion organ (β-human chorionic gonadotropin (β-hCG), steroids, vCTB fusion has to be tightly regulated since a limited fusion rate may lead to an abnormal STB layer formation and placental function deficit, whereas an accelerated fusion process would lead to the same phenotype due to a too rapid depletion of the regenerative pool of vCTB5.
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