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BioMed Research International
Volume 2014, Article ID 274507, 11 pages
Research Article

Potential Role of A2B Adenosine Receptors on Proliferation/Migration of Fetal Endothelium Derived from Preeclamptic Pregnancies

1Vascular Physiology Laboratory, Group of Investigation in Tumor Angiogenesis (GIANT), Group of Research and Innovation in Vascular Health (GRIVAS Health), Department of Basic Sciences, Faculty of Sciences, Universidad del Bío-Bío, Chillán, Chile
2Obstetrics and Gynecology Department, Herminda Martin Clinical Hospital, Chillan, Chile
3University of Queensland Centre for Clinical Research (UQCCR), Faculty of Medicine and Biomedical Sciences, University of Queensland, Herston, QLD 4006, Australia
4Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepción, Chile
5Cellular and Molecular Physiology Laboratory (CMPL), Division of Obstetrics and Gynecology, Faculty of Medicine, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile

Received 13 December 2013; Accepted 1 April 2014; Published 28 April 2014

Academic Editor: Gregory Rice

Copyright © 2014 Jesenia Acurio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


To investigate the functionality of adenosine receptor (AR) and the nitric oxide (NO) and vascular endothelial growth factor (VEGF) signaling pathway in the endothelial cell proliferation/migration during preeclampsia, we used human umbilical vein endothelial cells (HUVECs) isolated from normal pregnancies or pregnancies with preeclampsia . Experiments were performed in presence or absence of the nonselective adenosine receptor agonist NECA, the AR selective antagonist MRS-1754, and the nitric oxide synthase (NOS) inhibitor L-NAME. Results indicated that cells from preeclampsia exhibited a significant higher protein level of AR and logEC50 for NECA-mediated proliferation than normotensive pregnancies. The stimulatory effect of NECA (10 μM, 24 h) on cell proliferation was prevented by MRS-1754 (5 nM) coincubation only in cells from normotensive pregnancies. Nevertheless, L-NAME (100 μM, 24 h) reduced the NECA-induced cell proliferation/migration in HUVEC from normal pregnancy; however in preeclampsia only NECA-induced cell proliferation was reduced by L-NAME. Moreover, NECA increased protein nitration and abundance of VEGF in cells from normal pregnancy and effect prevented by MRS-1754 coincubation. Nevertheless, in preeclampsia NECA did not affect the protein level of VEGF. In conclusion HUVECs from preeclampsia exhibit elevated protein level of AR and impairment of AR-mediated NO/VEGF signaling pathway.