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dc.contributor.author
Sánchez Jiménez, F.
dc.contributor.author
Pérez Pérez, A.
dc.contributor.author
González Yanes, C.
dc.contributor.author
Varone, Cecilia Laura
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dc.contributor.author
Sánchez Margalet, V.
dc.date.available
2020-01-27T20:29:27Z
dc.date.issued
2011-06
dc.identifier.citation
Sánchez Jiménez, F.; Pérez Pérez, A.; González Yanes, C.; Varone, Cecilia Laura; Sánchez Margalet, V.; Sam68 mediates leptin-stimulated growth by modulating leptin receptor signaling in human trophoblastic JEG-3 cells; Oxford University Press; Human Reproduction; 26; 9; 6-2011; 2306-2315
dc.identifier.issn
0268-1161
dc.identifier.uri
http://hdl.handle.net/11336/95901
dc.description.abstract
Background Sam68, a member of the signal transduction and activation of RNA metabolism (STAR) family of RNA-binding proteins, has been previously implicated as an adaptor molecule in different signaling systems, including leptin receptor (LEPR) signaling. LEPR activation is known to stimulate JAK-STAT, MAPK and PI3K signaling pathways, thus mediating the biological effects of leptin in different cell types, including trophoblastic cells. We have recently found that leptin stimulation also promotes the overexpression and tyrosine phosphorylation of Sam68 in human trophoblastic JEG-3 cells, suggesting a role for Sam68 in leptin signaling and action in these cells. In the present work, we have studied the participation of Sam68 in the main signaling pathways activated by LEPR to increase growth and proliferation in trophoblastic JEG-3 cells. Methods We used an antisense strategy to down-regulate Sam68 expression in these cells, and we studied LEPR signaling by immunoprecipitation and poly-U affinity precipitation and by analyzing phosphorylation levels of signaling proteins by immunoblot. The effect of leptin on protein synthesis and proliferation was studied by 3[H]-leucine and 3[H]-thymidine incorporation. Results Sam68 knockdown impaired leptin activation of JAK-STAT, PI3K and MAPK signaling pathways in JEG-3 cells. We have also found that leptin-stimulated Sam68 tyrosine phosphorylation is dependent on JAK-2 activity, since the pharmacological inhibitor AG490 prevents the phosphorylation of Sam68 in JEG-3 cells. Finally, the trophic and proliferative effect of leptin in trophoblastic cells is dependent on Sam68 expression, since its down-regulation impaired the leptin-stimulated DNA and protein synthesis. Conclusions These data demonstrate that Sam68 participates in the main signaling pathways of LEPR to mediate the trophic and proliferative effect of leptin in human trophoblastic cells.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Oxford University Press
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
LEPR SIGNALING
dc.subject
LEPTIN
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PLACENTA
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SAM68
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TROPHOBLAST
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Sam68 mediates leptin-stimulated growth by modulating leptin receptor signaling in human trophoblastic JEG-3 cells
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-11-08T15:09:11Z
dc.journal.volume
26
dc.journal.number
9
dc.journal.pagination
2306-2315
dc.journal.pais
Reino Unido
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dc.journal.ciudad
Oxford
dc.description.fil
Fil: Sánchez Jiménez, F.. Universidad de Sevilla; España
dc.description.fil
Fil: Pérez Pérez, A.. Universidad de Sevilla; España
dc.description.fil
Fil: González Yanes, C.. Universidad de Sevilla; España
dc.description.fil
Fil: Varone, Cecilia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
dc.description.fil
Fil: Sánchez Margalet, V.. Universidad de Sevilla; España
dc.journal.title
Human Reproduction
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/humrep/article/26/9/2306/720090
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1093/humrep/der187
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