To investigate whether fetal endothelial cell proliferation and migration are modulated by the A 2A adenosine receptor (A 2A AR), nitric oxide (NO) and the vascular endothelial growth factor (VEGF) signaling pathway, we isolated human umbilical vein endothelial cells from normal pregnancy (n023), preterm delivery (n04), and late-onset (LOPE, n010) and early-onset preeclampsia (EOPE, n08). We used the non-selective adenosine receptor agonist (NECA) and the selective agonist (CGS-21680) and/or selective antagonist (ZM-241385) for A 2A AR. Also, the nitric oxide synthase (NOS) inhibitor, L-NAME, was used in co-incubation with CGS-21680. Compared to normal pregnancy, EOPE exhibited low cell proliferation and migration associated with reduced expressions of A 2A AR and VEGF and NO synthesis (i.e., total and phosphorylated serine 1177 endothelial NOS and nitrite formation). In contrast, LOPE exhibited the opposite behavior in all these markers compared to normal pregnancy or EOPE. Cell proliferation and migration were increased by CGS-21680 (or NECA) in all analyzed groups (EOPE>LO-PE>normal pregnancy) compared to their respective basal conditions, an effect that was associated with high NO and VEGF synthesis and blocked by ZM-241385 with significantly different IC 50 for each group (EOPE>LOPE>normal pregnancy). The differences seem independent of gestational age.L-NAME blocked the CGS-21680-mediated cell proliferation and migration in normal pregnancy and LOPE (IC 50 036.2± 2.5 and 8.6±2.2 nM, respectively) as well as the VEGF expression in normal pregnancy. Therefore, the A 2A AR/NO/ VEGF signaling pathway exhibits a pro-angiogenic effect in normal pregnancies and LOPE, whereas impairment in this pathway seems related to the reduced angiogenic capacity of the fetal endothelium in EOPE.

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There are no data regarding adenosine levels in obese children, even though is a ubiquitous molecule implicated in the regulation of lipid metabolism in humans. To determinate whether adenosine plasma levels are related with anthropometric and biochemical markers in children, we studied 51 students belong to Ramon Belmar School in Linares, Chile. Review of clinical data and frequent food questionnaire were taken in order to collect the information. Plasma adenosine levels were measured by high-performance liquid chromatography and biochemical parameters including insulin, glucose, total proteins, and lipid profile by using standard colorimetric assays. Children with detectable (above 0.1 μM) adenosine plasma levels (n = 30; BMI, 22.3 ± 0.7) had higher total cholesterol (P < 0.05); triglycerides (P < 0.01) and LDL-cholesterol (P < 0.05) concentrations than children with undetectable adenosine levels (n = 21; BMI, 23.9 ± 0.61). Among the analyzed variables, only BMI and BMI standard deviation score (BMI-SDS) were positively correlated with adenosine levels. Besides, obese children (n = 10) showed significantly high adenosine levels compared to controls (n = 11; 1.8 ± 0.2 vs. 1.2 ± 0.1 μM/mg protein, respectively. P < 0.05), but not compared to overweight children (n = 9). In conclusion, obesity in children is associated to high adenosine plasma levels. This study opens a new perspective to investigate the role of adenosine in the regulation of lipid metabolism in obese children.

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