Sagrillo-Fagundes, Lucas; Salustiano, Eugênia Maria Assuncao; Ruano, Rodrigo; Markus, Regina P. et Vaillancourt, Cathy . Promoting Healthy Lifestyles in Youth: Preliminary Findings from The Centre Pédiatrique d’Intervention en Prévention et en Réadaptation Cardiovasculaires (Circuit) Program In: Meeting of the International Federation of Placenta Associations (IFPA) 2018, 21-24 September 2018, Tokyo, Japon.
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Objectives: Human trophoblasts synthesize melatonin throughout the pregnancy. Placental disruptions impair the trophoblastic production of melatonin and also lead to increased autophagy, inflammation, and apoptosis. Exogenous melatonin has been suggested as a possible protective treatment against the deleterious effects of hypoxia/reoxygenation (H/R). However, in pregnancy complications, the effect of melatonin on inflammation and autophagy has never been investigated. The aim of this study was to determine how melatonin modulates inflammation and autophagy to increase the viability of the syncytiotrophoblast exposed to H/R, a model that mimics aberrant variations of oxygenation described in pregnancy disorders like preeclampsia.
Methods: Human primary villous cytotrophoblasts were isolated from normal term placentas and maintained in normoxia for 72h to induce the syncytialization into syncytiotrophoblast and then exposed to H/R (0.5% O2, 4h) or normoxia until 96h. During the same period, cells were exposed or not to 1mM melatonin every 24h. Inhibition of the NFkB activation was induced with 25mM PDTC during the last 24h of cell culture.
Results: H/R decreases endogenous melatonin synthesis and IL-10 productions, whereas it increases TNF, IL-6, and NFkB activation. In contrary, melatonin treatment increases ILe10 levels and restores the levels of TNF and IL-6 in H/R conditions. H/R upregulates the autophagy activation. Both melatonin and the inhibition of NFkB maximize the induction of autophagy and consequently increasesy the cell survival in H/R conditions.
Conclusion: Our results suggest that H/R, which is present in pregnancy complications such as pre-eclampsia, inhibits the endogenous melatonin production and reduces the viability of syncytiotrophoblast via the activation of pro-inflammatory factors. Exposure to exogenous melatonin induces both anti-inflammatory actions and autophagy to finally enhance the survival of the syncytiotrophoblast, which is a promising set of results that endorses the protective actions of melatonin on the placental homoeostasis.
| Type de document: | Document issu d'une conférence ou d'un atelier |
|---|---|
| Informations complémentaires: | Affiche scientifique P2.99 Placenta (2018) 69:e81 |
| Mots-clés libres: | - |
| Centre: | Centre INRS-Institut Armand Frappier |
| Date de dépôt: | 15 juill. 2021 14:39 |
| Dernière modification: | 15 juill. 2021 14:39 |
| URI: | https://espace.inrs.ca/id/eprint/11887 |
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