Regulation of leptin expression and its action in placental cells

JULIETA LORENA MAYMÓ; ANTONIO PÉREZ-PÉREZ; VICTOR SÁNCHEZ MARGALET; JUAN CARLOS CALVO; CECILIA VARONE

Foz de Iguazú

Congreso; XXXIX Annual Meeting of The Brazilian Biochemistry and Molecular Biology Society – SBBq; 2010

SBBq

Abstract Leptin, the peripheral signal produced by the adipocyte to regulate energy metabolism, can also be produced by placenta, where it may have a role as an autocrine and paracrine hormone. In the last past years it has been suggested to be involved in some functions during pregnancy such as growth, angiogenesis and immunomodulation. The molecular mechanisms involved in the adhesion of the embryos to uterine epithelium and growth are still unknown. We have demonstrated that leptin promotes proliferation and survival of trophoblastic cells. In the present work we aimed to study the regulation of leptin expression in placenta. BeWo and JEG-3 choriocarcinoma cell line, as well as trophoblastic cells from human placenta explants were used. Western blots, qRT-PCR and transient transfections experiments were carried out.We found that hCG has a stimulatory effect on endogenous leptin expression as well as in leptin promoter activity and in leptin mRNA expression. We determined that hCG effect could be partially blocked by pharmacologic inhibition of MAPK pathway with 50 uM PD98059. Moreover, hCG treatment promoted MAPK kinase and ERK1/ERK2 phosphorylation in placental cells. In conclusion,we provide some evidence suggesting that hCG induces leptin expression in trophoblastic cells probably involving the MAPK signal transduction pathway.Our results further support the importance of leptin in the biology of reproduction. demonstrated that leptin promotes proliferation and survival of trophoblastic cells. In the present work we aimed to study the regulation of leptin expression in placenta. BeWo and JEG-3 choriocarcinoma cell line, as well as trophoblastic cells from human placenta explants were used. Western blots, qRT-PCR and transient transfections experiments were carried out.We found that hCG has a stimulatory effect on endogenous leptin expression as well as in leptin promoter activity and in leptin mRNA expression. We determined that hCG effect could be partially blocked by pharmacologic inhibition of MAPK pathway with 50 uM PD98059. Moreover, hCG treatment promoted MAPK kinase and ERK1/ERK2 phosphorylation in placental cells. In conclusion,we provide some evidence suggesting that hCG induces leptin expression in trophoblastic cells probably involving the MAPK signal transduction pathway.Our results further support the importance of leptin in the biology of reproduction. demonstrated that leptin promotes proliferation and survival of trophoblastic cells. In the present work we aimed to study the regulation of leptin expression in placenta. BeWo and JEG-3 choriocarcinoma cell line, as well as trophoblastic cells from human placenta explants were used. Western blots, qRT-PCR and transient transfections experiments were carried out.We found that hCG has a stimulatory effect on endogenous leptin expression as well as in leptin promoter activity and in leptin mRNA expression. We determined that hCG effect could be partially blocked by pharmacologic inhibition of MAPK pathway with 50 uM PD98059. Moreover, hCG treatment promoted MAPK kinase and ERK1/ERK2 phosphorylation in placental cells. In conclusion,we provide some evidence suggesting that hCG induces leptin expression in trophoblastic cells probably involving the MAPK signal transduction pathway.Our results further support the importance of leptin in the biology of reproduction. . We have demonstrated that leptin promotes proliferation and survival of trophoblastic cells. In the present work we aimed to study the regulation of leptin expression in placenta. BeWo and JEG-3 choriocarcinoma cell line, as well as trophoblastic cells from human placenta explants were used. Western blots, qRT-PCR and transient transfections experiments were carried out.We found that hCG has a stimulatory effect on endogenous leptin expression as well as in leptin promoter activity and in leptin mRNA expression. We determined that hCG effect could be partially blocked by pharmacologic inhibition of MAPK pathway with 50 uM PD98059. Moreover, hCG treatment promoted MAPK kinase and ERK1/ERK2 phosphorylation in placental cells. In conclusion,we provide some evidence suggesting that hCG induces leptin expression in trophoblastic cells probably involving the MAPK signal transduction pathway.Our results further support the importance of leptin in the biology of reproduction.