Journal
BIOLOGY OF REPRODUCTION
Volume 80, Issue 6, Pages 1107-1114Publisher
OXFORD UNIV PRESS INC
DOI: 10.1095/biolreprod.108.070573
Keywords
adiponectin; adiponectin receptors; BeWo; cytokines; implantation; JEG-3; placenta; proliferation; signal transduction; trophoblast
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Funding
- Universite de Versailles-St-Quentin-en-Yvelines, France
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During embryo implantation, a complex dialog exists between the mother and the fetus. However, little is known about the molecules that participate in this process. Among various factors secreted at the maternal-fetal interface, the adipose tissue-derived leptin is now considered a placental growth factor. Adiponectin is another adipocyte-derived signaling molecule known to exert antiproliferative effects in various cell types. In this work, we studied adiponectin sensitivity and effects on JEG-3 and BeWo choriocarcinoma cell lines. First, we showed that JEG-3 and BeWo cells express the specific adiponectin receptors ADIPOR1 and ADIPOR2 and respond to human recombinant adiponectin by AMP-activated protein kinase (PRKA, also known as AMPK) activation. Second, we demonstrated that adiponectin induces a reduction in cell number and in [H-3]-thymidine incorporation, demonstrating that adiponectin has antiproliferative effects on trophoblastic cells. Furthermore, these effects of adiponectin seem to be, at least in part, mediated by the mitogen-activated protein kinase (MAPK) and phosphoinositide-3-kinase (PI3K) signaling pathways. We describe herein the direct effects of adiponectin in the control of trophoblastic cell proliferation.
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