To investigate the functionality ofA2Badenosine 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 pregnanciesn=15or pregnancies with preeclampsian=15. Experiments were performed in presence or absence of the nonselective adenosine receptor agonist NECA, theA2BAR 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 ofA2BAR and logEC50for 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 ofA2BAR and impairment ofA2BAR-mediated NO/VEGF signaling pathway.
Correction to Title, Results, and Conclusion in: Down-Regulated IncRNA F630028O10Rik Contributes to Suppress Lung Cancer in Mice Through Inhibiting miR-223-3p and VEGF Signaling Pathway
