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- W3084089522 abstract "Nox5 is the major ROS-generating Nox isoform in human vascular smooth muscle cells (VSMC). The role of Nox5 in oxidative stress and redox signaling underlying vascular dysfunction in hypertension is unclear. We examined molecular processes that regulate VSMC Nox5-induced ROS generation, focusing on c-Src. VSMC isolated from small arteries from normotensive (NT) and hypertensive (HT) subjects were studied. Nox5 expression and phosphorylation (immunoblotting, immunoprecipitation); ROS generation (chemiluminescence); activation of contractile signaling pathways (immunoblotting), Ca 2+ influx (Cal-520AM fluorescence), reversible protein oxidation (cysteine sulfenic acid probe BCN-E-BCN), actin polymerization (phalloidin staining) and migration (wound healing assay) were assessed in absence/presence of Nox5 (melittin) and Src (PP2) inhibitors. To study Nox5-specific effects, we used p22phox-silenced VSMCs (siRNA). Vascular function in VSMC-specific Nox5 transgenic mice was studied by wire myography. In HT, ROS levels (139±27%), Nox5 expression (103±23%) and phosphorylation were increased (77±17.93%) (p<0.05, vs NT). Activation of c-Src (101±26%), PKC (96±33%), MLC 20 (416±71%) and Ang II-induced Ca 2+ influx (574±44 vs NT:451±26) were also increased in HT (p<0.05, vs NT). Melittin reduced Ang II-induced ROS generation in both groups (p<0.05 vs Ctl). In contrast, p22phox silencing increased ROS in both groups, an effect blocked by melittin (p<0.05 vs Ctl). Nox5 inhibition reduced Ang II-induced c-Src phosphorylation and oxidation. In HT, p22phox silencing was associated with sustained Ang II-induced PKC (83±21% vs Ctl) and MLC 20 (89±22% vs Ctl) phosphorylation, effects blocked by melittin and PP2 (p<0.05 vs Ctl). Nox5 and c-Src inhibition reduced Ca 2+ influx, actin polymerization and migration in HT. Hypercontractility observed in Nox5 mice was abolished by melittin and PP2. Our findings demonstrate that Nox5 is upregulated in human hypertension. This is associated with activation of c-Src, increased redox signaling and VSMC cytoskeletal reorganization, migration and vascular contraction. We define a novel Nox5-ROS-c-Src signaling pathway that may play a role in vascular remodeling/dysfunction in hypertension." @default.
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- W3084089522 date "2020-09-01" @default.
- W3084089522 modified "2023-10-18" @default.
- W3084089522 title "Abstract P090: Nox5 Induces Vascular Damage Through C-src Activation In Human Hypertension" @default.
- W3084089522 doi "https://doi.org/10.1161/hyp.76.suppl_1.p090" @default.
- W3084089522 hasPublicationYear "2020" @default.
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