Potential role of A2B adenosine receptors on proliferation/migration of fetal endothelium derived from preeclamptic pregnancies

Acurio, Jesenia, Troncoso, Felipe, Bertoglia, Patricio, Salomon, Carlos, Aguayo, Claudio, Sobrevia, Luis and Escudero, Carlos (2014) Potential role of A2B adenosine receptors on proliferation/migration of fetal endothelium derived from preeclamptic pregnancies. BioMed Research International, 2014 . doi:10.1155/2014/274507


Author Acurio, Jesenia
Troncoso, Felipe
Bertoglia, Patricio
Salomon, Carlos
Aguayo, Claudio
Sobrevia, Luis
Escudero, Carlos
Title Potential role of A2B adenosine receptors on proliferation/migration of fetal endothelium derived from preeclamptic pregnancies
Formatted title
 Potential role of A2B adenosine receptors on proliferation/migration of fetal endothelium derived from preeclamptic pregnancies
Journal name BioMed Research International   Check publisher's open access policy
ISSN 2314-6141
2314-6133
Publication date 2014-04-28
Year available 2014
Sub-type Article (original research)
DOI 10.1155/2014/274507
Open Access Status DOI
Volume 2014
Total pages 11
Place of publication New York, NY, United States
Publisher Hindawi Publishing Corporation
Collection year 2015
Language eng
Formatted abstract
 To investigate the functionality of A2B adenosine receptor (A2BAR) 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 (n=15) or pregnancies with preeclampsia (n=15). Experiments were performed in presence or absence of the nonselective adenosine receptor agonist NECA, the A2BAR 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 A2BAR and logEC50 for NECA-mediated proliferation than normotensive pregnancies. The stimulatory effect of NECA (10µM, 24 h) on cell proliferation was prevented by MRS-1754 (5 nM) coincubation only in cells from normotensive pregnancies. Nevertheless, L-NAME (100µM, 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 A2BAR and impairment of A2BAR-mediated NO/VEGF signaling pathway.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Article ID 274507

Document type: Journal Article
Sub-type: Article (original research)
Collections: UQ Centre for Clinical Research Publications
Official 2015 Collection
 
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