We are analyzing https://link.springer.com/article/10.1007/s10753-004-6047-y.

Title:
RSV Causes HIF-1α Stabilization via NO Release in Primary Bronchial Epithelial Cells | Inflammation
Description:
RSV infection is characterized by airway edema. Stabilization of hypoxia inducible factor-1α (HIF-1α) is important in both inflammation and edema formation. In this study we evaluated whether RSV induced release of nitric oxide (NO) by bronchial airway epithelial cells leading to the stabilization of HIF-1α and subsequent transcription of VEGF165. Primary human bronchial epithelial cells (HBEpC) were used; cell supernatants were analyzed. Western blot analysis was used for the detection of HIF-1α. Bronchial airway epithelial monolayer permeability was assessed using electric cell-substrate impedance sensing (ECIS) in real time. There was increased stabilization of HIF-1α in RSV infected cells. Addition of an NO inhibitor blocked RSV mediated HIF-1α expression. Antagonism of NO also inhibited VEGF production and HBEpC monolayer permeability. Our results demonstrate that in HBEpC, RSV induced NO causes stabilization of HIF-1α in vitro.
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Keywords {🔍}

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Topics {✒️}

5-tetramethylimidazoline-1oxyl-3-oxide sodium salt o2-regulated gene expression o2-sensing protein hydroxylases hypoxia-inducible transcription factors month download article/chapter hypoxia-inducible factor-1 expression hypoxia inducible factor-1α rous-whipple award lecture hypoxia-inducible factor-1 activity hypoxia inducible factor-1alpha o2-regulated prolyl hydroxylation myeloid cell-mediated inflammation airway epithelial cells hypoxia-inducible factor 1 hypoxia-inducible-factor 1 inhibited vegf production vhl-mediated destruction airway epithelial injury hbepc monolayer permeability privacy choices/manage cookies rsv infected cells highly involved factor full article pdf respiratory syncytial virus article inflammation aims nitric oxide synthase hypoxia response element angiogenic response induced tumor stroma generation european economic area altered redox states murine peritoneal macrophages pi 3k pathway normal adult tissues mammalian o2 homeostasis rsv induced release conditions privacy policy carboxy ptio dna-binding activity western blot analysis oxygen-dependent proteolysis human disease gels induce angiogenesis critical care medicine accepting optional cookies redox-dependent effect airway edema rsv infection journal finder publish hif-1α stabilization

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         description:RSV infection is characterized by airway edema. Stabilization of hypoxia inducible factor-1α (HIF-1α) is important in both inflammation and edema formation. In this study we evaluated whether RSV induced release of nitric oxide (NO) by bronchial airway epithelial cells leading to the stabilization of HIF-1α and subsequent transcription of VEGF165. Primary human bronchial epithelial cells (HBEpC) were used; cell supernatants were analyzed. Western blot analysis was used for the detection of HIF-1α. Bronchial airway epithelial monolayer permeability was assessed using electric cell-substrate impedance sensing (ECIS) in real time. There was increased stabilization of HIF-1α in RSV infected cells. Addition of an NO inhibitor blocked RSV mediated HIF-1α expression. Antagonism of NO also inhibited VEGF production and HBEpC monolayer permeability. Our results demonstrate that in HBEpC, RSV induced NO causes stabilization of HIF-1α in vitro.
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      description:RSV infection is characterized by airway edema. Stabilization of hypoxia inducible factor-1α (HIF-1α) is important in both inflammation and edema formation. In this study we evaluated whether RSV induced release of nitric oxide (NO) by bronchial airway epithelial cells leading to the stabilization of HIF-1α and subsequent transcription of VEGF165. Primary human bronchial epithelial cells (HBEpC) were used; cell supernatants were analyzed. Western blot analysis was used for the detection of HIF-1α. Bronchial airway epithelial monolayer permeability was assessed using electric cell-substrate impedance sensing (ECIS) in real time. There was increased stabilization of HIF-1α in RSV infected cells. Addition of an NO inhibitor blocked RSV mediated HIF-1α expression. Antagonism of NO also inhibited VEGF production and HBEpC monolayer permeability. Our results demonstrate that in HBEpC, RSV induced NO causes stabilization of HIF-1α in vitro.
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