Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells

Leptin is produced in placenta where it has been found to be an important autocrine signal for trophoblastic growth during pregnancy, promoting antiapoptotic and trophic effects. Leptin receptor is present in trophoblastic cells and leptin may fully activate signaling. We have previously implicated...

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Autores principales: Sánchez-Jiménez, F., Pérez-Pérez, A., González-Yanes, C., Najib, S., Varone, C.L., Sánchez-Margalet, V.
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Acceso en línea:http://hdl.handle.net/20.500.12110/paper_03037207_v332_n1-2_p221_SanchezJimenez
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spelling todo:paper_03037207_v332_n1-2_p221_SanchezJimenez2023-10-03T15:19:52Z Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells Sánchez-Jiménez, F. Pérez-Pérez, A. González-Yanes, C. Najib, S. Varone, C.L. Sánchez-Margalet, V. Leptin receptor Placenta Sam68 Signal transduction leptin leptin receptor protein Sam68 RNA article cell activation cell level controlled study dose response down regulation hormonal regulation human human cell priority journal protein expression protein function protein phosphorylation protein RNA binding protein synthesis signal transduction trophoblast Adaptor Proteins, Signal Transducing Cell Line Choriocarcinoma DNA-Binding Proteins Female Humans Leptin Phosphorylation Placenta Pregnancy Receptors, Leptin RNA-Binding Proteins Signal Transduction Trophoblasts Tyrosine Leptin is produced in placenta where it has been found to be an important autocrine signal for trophoblastic growth during pregnancy, promoting antiapoptotic and trophic effects. Leptin receptor is present in trophoblastic cells and leptin may fully activate signaling. We have previously implicated the RNA-binding protein Sam68 in leptin signal transduction in immune cells. In the present work, we have studied the possible role of Sam68 in leptin receptor signaling in trophoblastic cells (JEG-3 cells). Leptin dose-dependently stimulated Sam68 phosphorylation in JEG-3 cells, as assessed by immunoprecipitation and immunoblot with anti-phosphotyrosine antibodies. As previously observed in other systems, tyrosine phosphorylation of Sam68 in response to leptin inhibits its RNA binding capacity. Besides, leptin stimulation dose-dependently increases Sam68 expression in JEG-3 cells, as assessed by quantitative PCR. Consistently, the amount of Sam68 protein is increased after 24. h of leptin stimulation of trophoblastic cells. In order to study the possible role of Sam68 on leptin receptor synthesis, we employed antisense strategy to knockdown the expression of Sam68. We have found that a decrease in Sam68 expression leads to a decrease in leptin receptor amount in JEG-3 cells, as assessed both by quantitative PCR and immunoblot.These results strongly suggest the participation of Sam68 in leptin receptor signaling in human trophoblastic cells, and therefore, Sam68 may mediate some of the leptin effects in placenta. © 2010 Elsevier Ireland Ltd. Fil:Varone, C.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_03037207_v332_n1-2_p221_SanchezJimenez
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Leptin receptor
Placenta
Sam68
Signal transduction
leptin
leptin receptor
protein Sam68
RNA
article
cell activation
cell level
controlled study
dose response
down regulation
hormonal regulation
human
human cell
priority journal
protein expression
protein function
protein phosphorylation
protein RNA binding
protein synthesis
signal transduction
trophoblast
Adaptor Proteins, Signal Transducing
Cell Line
Choriocarcinoma
DNA-Binding Proteins
Female
Humans
Leptin
Phosphorylation
Placenta
Pregnancy
Receptors, Leptin
RNA-Binding Proteins
Signal Transduction
Trophoblasts
Tyrosine
spellingShingle Leptin receptor
Placenta
Sam68
Signal transduction
leptin
leptin receptor
protein Sam68
RNA
article
cell activation
cell level
controlled study
dose response
down regulation
hormonal regulation
human
human cell
priority journal
protein expression
protein function
protein phosphorylation
protein RNA binding
protein synthesis
signal transduction
trophoblast
Adaptor Proteins, Signal Transducing
Cell Line
Choriocarcinoma
DNA-Binding Proteins
Female
Humans
Leptin
Phosphorylation
Placenta
Pregnancy
Receptors, Leptin
RNA-Binding Proteins
Signal Transduction
Trophoblasts
Tyrosine
Sánchez-Jiménez, F.
Pérez-Pérez, A.
González-Yanes, C.
Najib, S.
Varone, C.L.
Sánchez-Margalet, V.
Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
topic_facet Leptin receptor
Placenta
Sam68
Signal transduction
leptin
leptin receptor
protein Sam68
RNA
article
cell activation
cell level
controlled study
dose response
down regulation
hormonal regulation
human
human cell
priority journal
protein expression
protein function
protein phosphorylation
protein RNA binding
protein synthesis
signal transduction
trophoblast
Adaptor Proteins, Signal Transducing
Cell Line
Choriocarcinoma
DNA-Binding Proteins
Female
Humans
Leptin
Phosphorylation
Placenta
Pregnancy
Receptors, Leptin
RNA-Binding Proteins
Signal Transduction
Trophoblasts
Tyrosine
description Leptin is produced in placenta where it has been found to be an important autocrine signal for trophoblastic growth during pregnancy, promoting antiapoptotic and trophic effects. Leptin receptor is present in trophoblastic cells and leptin may fully activate signaling. We have previously implicated the RNA-binding protein Sam68 in leptin signal transduction in immune cells. In the present work, we have studied the possible role of Sam68 in leptin receptor signaling in trophoblastic cells (JEG-3 cells). Leptin dose-dependently stimulated Sam68 phosphorylation in JEG-3 cells, as assessed by immunoprecipitation and immunoblot with anti-phosphotyrosine antibodies. As previously observed in other systems, tyrosine phosphorylation of Sam68 in response to leptin inhibits its RNA binding capacity. Besides, leptin stimulation dose-dependently increases Sam68 expression in JEG-3 cells, as assessed by quantitative PCR. Consistently, the amount of Sam68 protein is increased after 24. h of leptin stimulation of trophoblastic cells. In order to study the possible role of Sam68 on leptin receptor synthesis, we employed antisense strategy to knockdown the expression of Sam68. We have found that a decrease in Sam68 expression leads to a decrease in leptin receptor amount in JEG-3 cells, as assessed both by quantitative PCR and immunoblot.These results strongly suggest the participation of Sam68 in leptin receptor signaling in human trophoblastic cells, and therefore, Sam68 may mediate some of the leptin effects in placenta. © 2010 Elsevier Ireland Ltd.
format JOUR
author Sánchez-Jiménez, F.
Pérez-Pérez, A.
González-Yanes, C.
Najib, S.
Varone, C.L.
Sánchez-Margalet, V.
author_facet Sánchez-Jiménez, F.
Pérez-Pérez, A.
González-Yanes, C.
Najib, S.
Varone, C.L.
Sánchez-Margalet, V.
author_sort Sánchez-Jiménez, F.
title Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title_short Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title_full Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title_fullStr Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title_full_unstemmed Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title_sort leptin receptor activation increases sam68 tyrosine phosphorylation and expression in human trophoblastic cells
url http://hdl.handle.net/20.500.12110/paper_03037207_v332_n1-2_p221_SanchezJimenez
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