Dépôt numérique

In vitro model of preeclampsia: melatonin inhibits inflammation in human primary trophoblast cells

Assuncao Salustiano, Eugania Maria, Sagrillo-Fagundes, Lucas et Vaillancourt, Cathy . In vitro model of preeclampsia: melatonin inhibits inflammation in human primary trophoblast cells In: 12ème colloque du centre de recherche Biomed, 5 mai 2016, Centre de congrès Palace, Laval (Québec).

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Melatonin is produced by placenta and protects villous trophoblasts against hypox- ia/reoxygenation (H/R) - induced oxidative stress and apoptosis. However, melatonin’s anti - inflammatory activity in villous trophoblasts under H/R has never been investigated.

Objective: Determine if melatonin decreases inflammation in our in vitro model of primary villous trophoblasts culture under H/R, which mimics preeclampsia.

Methods : Human villous cytotrophoblast (vCTB) were isolated from normal term placentas and maintained under culture for 72 hours in normoxia to induce differentiation in syncytiotrophoblast, and after exposed to normoxia or H/R. vCTB were treated with: melatonin (1mM), LPS (1mg/mL) or siAANAT (limiting melatonin synthetizing - enzyme). Pro and anti - inflammatory cytokines (TNF α, IL - 6, IL - 10), and melatonin were measured by ELISA. Cells are also treated with treated with melatonin, bafilomycin (autophagy inhibitor), or had melatonin receptors (MT1/MT2) supressed with siRNA.

Results: Melatonin levels are reduced in vCTB under H/R compared to normoxia. Melatonin levels are increased in vCTB treated with melatonin. TNF - α is decreased in vCTB treated with melatonin in normoxia and H/R (50%) (P≤0.05). IL - 10 is in- creased of 3 - fold (P≤0.01) in vCTB treated with melatonin compared with siAANAT in normoxia and IL - 6 is increased 3 - fold (P≤0.01). HR activates Nf κ B pathway in- creasing inflammation and; treatment with melatonin increased autophagy markers LC3BII as well as Beclin1; suggesting melatonin activates autophagy.

Conclusion : This study confirms that melatonin protects trophoblast by the modula- tion of autophagy and inflammation pathways, which are highly implicated in preeclampsia and fetal development. With the current clinical - trials to treat preeclampsia with melatonin, deeper comprehension of its effect on trophoblasts is required.

Type de document: Document issu d'une conférence ou d'un atelier
Informations complémentaires: Présentation par affiche
Mots-clés libres: -
Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 25 déc. 2017 21:53
Dernière modification: 25 déc. 2017 21:53
URI: https://espace.inrs.ca/id/eprint/6615

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