Molecular Human Reproduction, Vol. 9, No. 7, 395-398,
July 2003
© 2003 European Society of Human Reproduction and Embryology
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Modulation of placental vascular endothelial growth factor by leptin and hCG
Submitted on April 17, 2002; resubmitted on February 5, 2003. accepted on March 28, 2003
Department of Obstetrics and Gynaecology, Clinic of Infertility and Gynaecological Endocrinology–WHO Collaborating Centre in Human Reproduction, University Hospital of Geneva, 32 Boulevard de la Cluse, 1211 Geneva, Switzerland
1 To whom correspondence should be addressed at: Clinique de Stérilité et d’Endocrinologie Gynécologique, Hôpital Cantonal Universitaire de Genève, 32, Boulevard de la Cluse, 1211 Genève 14, Switzerland. e-mail: paul.bischof{at}hcuge.ch
Vascular endothelial growth factor (VEGF) has been identified as an endothelium-specific mitogen and inducer of angiogenesis and endothelial cell survival. Leptin and hCG have also been suggested as possible regulators of angiogenesis in various models. In-vivo and in-vitro assays revealed that leptin has an angiogenic activity and that the vascular endothelium is a target for leptin. Thus, we hypothesized that products of cytotrophoblastic cells may play a role in placental angiogenesis and we therefore investigated the effects of leptin and hCG on cytotrophoblast VEGF secretion. We incubated cytotrophoblastic cells (CTB) with recombinant human leptin (rhLept) (0–4 pg/ml) or hCG (0–30 000 IU/ml) for 4 h. rhLept significantly stimulated hCG (P = 0.0045) and decreased VEGF release (P = 0.0008) by CTB in a concentration-dependent manner. On the other hand, increasing concentrations of hCG (0–30 000 IU/ml), induced a significant inhibition of leptin secretion (P = 0.0028) and a marked dose-dependent stimulation of VEGF165 secretion (P < 0.0001). We observed an increase of >1000-fold in basal trophoblastic VEGF secretion with physiological concentrations of hCG in vitro. An inhibitory effect of hCG on trophoblastic leptin secretion was also observed, suggesting that hCG might exert a possible negative feedback on trophoblastic release of leptin. We hypothesize that trophoblastic products such as hCG and leptin are probably involved in the control of VEGF secretion at the maternal–fetal interface.
Key words: angiogenesis/hCG/leptin/trophoblast/VEGF
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