Leptin protects placental cells from apoptosis induced by acidic stress
Development of the human placenta is critical for a successful pregnancy. The placenta allows the exchange of oxygen and carbon dioxide and is crucial to manage acid-base balance within a narrow pH. It is known that low pH levels are a risk of apoptosis in several tissues. However, there has been li...
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Springer Verlag
2019
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| 100 | 1 | |a Pérez-Pérez, A. | |
| 245 | 1 | 0 | |a Leptin protects placental cells from apoptosis induced by acidic stress |
| 260 | |b Springer Verlag |c 2019 | ||
| 270 | 1 | 0 | |m Sánchez-Margalet, V.; Department of Medical Biochemistry and Molecular Biology and Immunology, School of Medicine, Virgen Macarena University Hospital, University of Seville, Av. Dr. Fedriani 3, Spain; email: margalet@us.es |
| 506 | |2 openaire |e Política editorial | ||
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| 520 | 3 | |a Development of the human placenta is critical for a successful pregnancy. The placenta allows the exchange of oxygen and carbon dioxide and is crucial to manage acid-base balance within a narrow pH. It is known that low pH levels are a risk of apoptosis in several tissues. However, there has been little discussion about the effect of acidic stress in the placenta. Leptin is produced by the placenta with a trophic autocrine effect. Previous results of our group have demonstrated that leptin prevents apoptosis of trophoblast cells under different stress conditions such as serum deprivation and hyperthermia. The purpose of the present work is to evaluate acidic stress consequences in trophoblast explant survival and to determine leptin action in these conditions. For this objective, term human trophoblast explants were cultured at physiological pH (pH 7.4) and at acidic pH (pH 6.8) in the presence or absence of leptin. Western blot assays were performed to study the abundance of active caspase-3 and the p89 fragment of PARP-1. Pro-apoptotic and pro-survival members of Bcl-2 family, as Bax, t-Bid, and Bcl-2, were studied. Moreover, p53 pathway was also evaluated including Mdm-2, the main p53 regulator. Active caspase-3 and cleaved PARP-1 abundances were increased at low extracellular pH. Moreover, t-Bid levels were also augmented as well as p53 expression and phosphorylation on S46. Leptin treatment prevents the consequences of acidosis, decreasing p53 expression and increasing Mdm-2 expression. In summary, this work demonstrated for first time that low pH induces apoptosis of human trophoblast explants involving apoptotic intrinsic pathway, and leptin impairs this effect. © 2018, Springer-Verlag GmbH Germany, part of Springer Nature. |l eng | |
| 536 | |a Detalles de la financiación: Fondazione ART per la Ricerca sui Trapianti | ||
| 536 | |a Detalles de la financiación: Instituto de Salud Carlos III, PS09/00119, PI12/01172 | ||
| 536 | |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas | ||
| 536 | |a Detalles de la financiación: Funding information This work was supported by a grant from the Instituto de Salud Carlos III (PS09/00119 and PI12/01172), funded in part by FEDER Funds, and ART is supported by a CONICET fellowship. | ||
| 593 | |a Department of Medical Biochemistry and Molecular Biology and Immunology, School of Medicine, Virgen Macarena University Hospital, University of Seville, Av. Dr. Fedriani 3, Seville, 41071, Spain | ||
| 593 | |a Laboratory of Placental Molecular Physiology, Department of Biological Chemistry, School of Sciences, University of Buenos Aires, IQUIBICEN-CONICET, Ciudad Universitaria, Pab. 2, Buenos Aires, Argentina | ||
| 593 | |a Department of Obstetrics and gynecology, Virgen Macarena University Hospital, University of Seville, Seville, Spain | ||
| 690 | 1 | 0 | |a ACIDIC STRESS |
| 690 | 1 | 0 | |a APOPTOSIS |
| 690 | 1 | 0 | |a LEPTIN |
| 650 | 1 | 7 | |2 spines |a PLACENTA |
| 700 | 1 | |a Toro, A. | |
| 700 | 1 | |a Vilariño-Garcia, T. | |
| 700 | 1 | |a Guadix, P. | |
| 700 | 1 | |a Maymó, J. | |
| 700 | 1 | |a Dueñas, J.L. | |
| 700 | 1 | |a Varone, C. | |
| 700 | 1 | |a Sánchez-Margalet, V. | |
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