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• W2158643268 abstract "Similar to infants born with persistent pulmonary hypertension of the newborn (PPHN), there is an increase in circulating endothelin-1 (ET-1) and decreased endothelial nitric oxide synthase (eNOS) gene expression in an ovine model of PPHN. These abnormalities lead to vasoconstriction and vascular remodeling. Our previous studies have demonstrated that reactive oxygen species (ROS) levels are elevated in the pulmonary arteries from PPHN lambs and that ET-1 increases ROS production in pulmonary arterial smooth muscle cells (PASMC) in culture. Thus the objective of this study was to determine whether there was a feedback mechanism between the ET-1-mediated increase in ROS in fetal PASMC (FPASMC) and a decrease in eNOS gene expression in fetal pulmonary arterial endothelial cells (FPAEC). Our results indicate that ET-1 increased H 2 O 2 levels in FPASMC in an endothelin A receptor-dependent fashion. This was observed in both FPASMC monoculture and in cocultures of FPASMC and FPAEC. Conversely, ET-1 decreased H 2 O 2 levels in FPAEC monoculture in an endothelin B receptor-dependent fashion. Furthermore, ET-1 decreased eNOS promoter activity by 40% in FPAEC in coculture with FPASMC. Promoter activity was restored in the presence of catalase. In FPAEC in monoculture treated with 0–100 μM H 2 O 2 , 12 μM had no effect on eNOS promoter activity, but it increased eNOS protein levels by 50%. However, at 100 μM, H 2 O 2 decreased eNOS promoter activity and protein levels in FPAEC by 79 and 40%, respectively. These data suggest a role for smooth muscle cell-derived H 2 O 2 in ET-1-mediated downregulation of eNOS expression in children born with PPHN." @default.
• W2158643268 created "2016-06-24" @default.
• W2158643268 creator A5016644607 @default.
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• W2158643268 date "2005-03-01" @default.
• W2158643268 modified "2023-10-15" @default.
• W2158643268 title "Endothelin-1 decreases endothelial NOS expression and activity through ET_A receptor-mediated generation of hydrogen peroxide" @default.
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• W2158643268 doi "https://doi.org/10.1152/ajplung.00283.2004" @default.
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