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EDN3 — NOX5

Text-mined interactions from Literome

Rask-Madsen et al., Arterioscler Thromb Vasc Biol 2005 (Arteriosclerosis...) : Furthermore, the review summarizes studies that implicate PKC in promoting proatherogenic mechanisms or inhibiting antiatherogenic mechanisms, including studies of endothelial dysfunction ; gene induction and activation of vascular NAD ( P ) H oxidase ; endothelial nitric oxide synthase expression and function ; endothelin-1 expression ; growth, migration, and apoptosis of vascular smooth muscle cells ; induction of adhesion molecules ; and oxidized low-density lipoprotein uptake by monocyte derived macrophages
Cheng et al., Acta Pharmacol Sin 2009 (Hypertrophy) : We hypothesized that dispersed NADPH oxidase , protein kinase Cepsilon ( PKCepsilon ), early response gene (ERG), and matrix metalloproteinase 9(MMP-9) across the heart by isoproterenol ( ISO ) medication might be mediated by the endothelin ( ET ) - ROS pathway
Pandey et al., Am J Physiol Heart Circ Physiol 2012 : In HVSMC, angiotensin II, endothelin-1 and TNF-a increased endogenous Nox5 mRNA levels, while adenovirus mediated overexpression of Nox5 promoted p38 MAPK, JAK2, JNK, and ERK1/2 phosphorylation in endothelial cells ( EC ), but only increased ERK1/2 phosphorylation in HVSMC
Hirata et al., J Cardiovasc Pharmacol 1993 : ET-1 and ET-3 rapidly ( within 1 min ) and dose-dependently ( 10 ( -10 ) to 10 ( -7 ) M ) stimulated production of nitrate/nitrite ( NOx ) in bovine EC ; ET-3 was more potent than ET-1 at generating endothelial NOx ... The ET-3 stimulated NOx production was completely abolished by a NO synthase inhibitor NG-monomethyl-L-arginine ( L-NMMA ), the effect of which was reversed by coadministration of excess L-arginine ... A selective calmodulin inhibitor W-7 dose-dependently inhibited the ET-3 stimulated NOx production, whereas a nonselective calmodulin inhibitor W-5 failed to affect NOx production