Leptin prevents apoptosis of trophoblastic cells by activation of MAPK pathway

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Leptin (Ob), the peripheral signal produced by the adipocyte to regulate energy metabolism, can also be produced by placenta, where it may work as an autocrine hormone. Recently, we have demonstrated that leptin promotes proliferation and survival of trophoblastic cells. In the present work we aimed...

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Detalles Bibliográficos
Autor principal: Pérez-Pérez, A.
Otros Autores: Maymó, J., Dueñas, J.L, Goberna, R., Calvo, J.C, Varone, C., Sánchez-Margalet, V.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2008
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PLACENTA
Acceso en línea:Registro en Scopus
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Biblioteca Central Dr. Luis F. Leloir (FCEN) de Universidad de Buenos Aires
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270 1 0 |m Sánchez-Margalet, V.; Departamento de Bioquímica Médica y Biología Molecular, Facultad de Medicina Hospital Universitario Virgen Macarena, Universidad de Sevilla, España, Spain; email: margalet@us.es 
506 |2 openaire  |e Política editorial 
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520 3 |a Leptin (Ob), the peripheral signal produced by the adipocyte to regulate energy metabolism, can also be produced by placenta, where it may work as an autocrine hormone. Recently, we have demonstrated that leptin promotes proliferation and survival of trophoblastic cells. In the present work we aimed to study the signal transduction pathways that mediate the trophic effect of leptin in placenta, by using the human placenta choriocarcinoma JEG-3 cell line, as well as trophoblastic cells from human placenta. We have assayed the early phase of apoptosis, triggered by serum deprivation, by using Annexin V-propidium iodide (PI) labeling and flow cytometric analysis, as well as the late phase of apoptosis by studying the activation of caspase-3. We have studied the major signalling pathways known to be triggered by the leptin receptor, and we have investigated the relative importance of these pathways in the effect of leptin by using pharmacological inhibitors. We have found that leptin stimulates Janus kinase (JAK)-signal transducers and activators of transcription (STAT) pathway by promoting JAK-2 and STAT-3 tyrosine phosphorylation. We have also demonstrated the activation of mitogen-activated protein kinase (MAPK) pathway by studying phosphorylation of extracellular-signal regulated kinase (Erk) kinase (MEK) and Erk1/2. PI3K pathway is also triggered by leptin stimulation as assessed by the study of protein kinase B (PKB) phosphorylation. These signaling pathways were confirmed in trophoblastic cells obtained from placenta of healthy donors. The effect of leptin on JEG-3 survival was completely reversed by blocking Erk1/2 activation employing the MEK inhibitor PD98059, whereas it was not affected by PI3K inhibition using wortmannin. These data suggest that the leptin antiapoptotic effect in placenta is mediated by the MAPK pathway. © 2008 Elsevier Inc. All rights reserved.  |l eng 
536 |a Detalles de la financiación: 75/06 
536 |a Detalles de la financiación: Instituto de Salud Carlos III, ISCIII CM07/00025 
536 |a Detalles de la financiación: This work was supported by a grant from Consejeria de Salud (75/06), Junta de Andalucía, Spain. Antonio Pérez-Pérez is a research fellow supported by the Instituto de Salud Carlos III (Contrato Post-formación especializada), ISCIII CM07/00025, Spain. 
593 |a Departamento de Bioquímica Médica y Biología Molecular, Facultad de Medicina Hospital Universitario Virgen Macarena, Universidad de Sevilla, España, Spain 
593 |a Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina 
593 |a Servicio de Ginecología y Obstetricia, Hospital Universitario Virgen Macarena, Universidad de Sevilla, España, Spain 
690 1 0 |a APOPTOSIS 
690 1 0 |a LEPTIN 
690 1 0 |a LEPTIN RECEPTOR 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a CASPASE 3 
690 1 0 |a JANUS KINASE 
690 1 0 |a JANUS KINASE 2 
690 1 0 |a LEPTIN 
690 1 0 |a LEPTIN RECEPTOR 
690 1 0 |a LIPOCORTIN 5 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE 
690 1 0 |a PROPIDIUM IODIDE 
690 1 0 |a PROTEIN KINASE B 
690 1 0 |a STAT PROTEIN 
690 1 0 |a STAT3 PROTEIN 
690 1 0 |a APOPTOSIS 
690 1 0 |a ARTICLE 
690 1 0 |a CELL ACTIVATION 
690 1 0 |a CELL LINE 
690 1 0 |a CHORIOCARCINOMA 
690 1 0 |a FLOW CYTOMETRY 
690 1 0 |a HUMAN 
690 1 0 |a HUMAN CELL 
690 1 0 |a PHOSPHORYLATION 
690 1 0 |a PREVENTION AND CONTROL 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a PROTEIN PHOSPHORYLATION 
690 1 0 |a TROPHOBLAST 
690 1 0 |a APOPTOSIS 
690 1 0 |a CELL LINE 
690 1 0 |a DOSE-RESPONSE RELATIONSHIP, DRUG 
690 1 0 |a ENZYME ACTIVATION 
690 1 0 |a HUMANS 
690 1 0 |a LEPTIN 
690 1 0 |a MAP KINASE SIGNALING SYSTEM 
690 1 0 |a TROPHOBLASTS 
650 1 7 |2 spines  |a PLACENTA 
650 1 7 |2 spines  |a PLACENTA 
700 1 |a Maymó, J. 
700 1 |a Dueñas, J.L. 
700 1 |a Goberna, R. 
700 1 |a Calvo, J.C. 
700 1 |a Varone, C. 
700 1 |a Sánchez-Margalet, V. 
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