The fine-tuning of endoplasmic reticulum stress response and autophagy activation during trophoblast syncytialization
| Autor: | Nolwenn Morris, Lucile Yart, Daniel Bastida-Ruiz, Manuella Epiney, Begoña Martinez de Tejada, Marie Cohen, Christine Wuillemin, Pascale Ribaux |
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| Rok vydání: | 2019 |
| Předmět: |
Cancer Research
Chaperone-mediated autophagy Blotting Western Immunology Cell Fluorescent Antibody Technique In Vitro Techniques Article Cellular and Molecular Neuroscience Syncytiotrophoblast Pregnancy Placenta Autophagy medicine Humans RNA Small Interfering lcsh:QH573-671 Cells Cultured reproductive and urinary physiology Fetus ddc:618 lcsh:Cytology Chemistry Endoplasmic reticulum Trophoblast Cell Differentiation Cell Biology Endoplasmic Reticulum Stress Trophoblasts Cell biology medicine.anatomical_structure Differentiation embryonic structures Beclin-1 Female Homeostasis |
| Zdroj: | Cell Death and Disease, Vol 10, Iss 9, Pp 1-15 (2019) Cell Death & Disease, Vol. 10, No 9 (2019) P. 651 Cell Death & Disease |
| ISSN: | 2041-4889 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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