VIP regulates glucose transport by human trophoblast-derived cells

F MERECH; R RAMHORST; V HAUK; D VOTA; C PÉREZ LEIRÓS; D PAPARINI

Mar del Plata

Congreso; LXI Reunón Anual SAIC; 2016

SAIC-SAI

The transport of nutrients across the placenta is strictly regulated and deficiencies in metabolism and transport of several factors like glucose, aminoacids and lipids are associated to intrauterine growth restriction (IUGR), large for gestational age newborns, among other complications. Glucose is the major energy substrate for the placenta and the fetus. Its transfer to the fetus is regulated by maternal levels, placental glucose metabolism and facilitated transport through Glut carrier proteins. Glut 1 appears to be the primary transporter and is found at both the maternal and the fetal-facing trophoblast membrane. The vasoactive intestinal peptide (VIP) is a pleiotropic neuropeptide that was shown to inhibit glucose oxidation in rat enterocytes. On the other hand, we have previously demonstrated that VIP is synthesized by human first and thirst trimester trophoblast (Tb) cells and favors Tb cell migration and invasion, two main processes required for placentation. Based on these evidences, the aim of the present work was to study the role of VIP and its receptors in the regulation of glucose transport bv Tb cells. We used two human Tb derived cell lines, Swan71 and BeWo cultured with/without VIP (10-100nM) for different times. We evaluated the expression of GLUT1 by qRT-PCR, glucose uptake by flow cytometry using the glucose fluorescent analog 2-NBDG and glucose transcellular transport on monolayer by means of transwell systems. Same assays were carried out in VIP knocked down Tb cells by VIP siRNA transfection. Our results show that VIP induced GLUT 1 mRNA expression at 7h (BeWo: 50nM VIP showed an increment of 31± 3 % respect to basal expression, n=3, p