RSV causes HIF-1α stabilization via NO release in primary bronchial epithelial cells

Muna M. Kilani, Kamal A. Mohammed, Najmunnisa Nasreen, Robert Tepper, Veena B. Antony

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

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 VEGF 165. 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.

Original languageEnglish
Pages (from-to)245-251
Number of pages7
JournalInflammation
Volume28
Issue number5
DOIs
StatePublished - Oct 2004

Fingerprint

Hypoxia-Inducible Factor 1
Nitric Oxide
Epithelial Cells
Permeability
Edema
Electric Impedance
Vascular Endothelial Growth Factor A
Western Blotting
Inflammation
Infection

Keywords

  • Carboxy-PTIO
  • ECIS
  • Edema
  • VEGF

ASJC Scopus subject areas

  • Medicine(all)
  • Immunology
  • Cell Biology

Cite this

RSV causes HIF-1α stabilization via NO release in primary bronchial epithelial cells. / Kilani, Muna M.; Mohammed, Kamal A.; Nasreen, Najmunnisa; Tepper, Robert; Antony, Veena B.

In: Inflammation, Vol. 28, No. 5, 10.2004, p. 245-251.

Research output: Contribution to journalArticle

Kilani, Muna M. ; Mohammed, Kamal A. ; Nasreen, Najmunnisa ; Tepper, Robert ; Antony, Veena B. / RSV causes HIF-1α stabilization via NO release in primary bronchial epithelial cells. In: Inflammation. 2004 ; Vol. 28, No. 5. pp. 245-251.
@article{07cb793353e841e1a00ee96f76016843,
title = "RSV causes HIF-1α stabilization via NO release in primary bronchial epithelial cells",
abstract = "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 VEGF 165. 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.",
keywords = "Carboxy-PTIO, ECIS, Edema, VEGF",
author = "Kilani, {Muna M.} and Mohammed, {Kamal A.} and Najmunnisa Nasreen and Robert Tepper and Antony, {Veena B.}",
year = "2004",
month = "10",
doi = "10.1007/s10753-004-6047-y",
language = "English",
volume = "28",
pages = "245--251",
journal = "Inflammation",
issn = "0360-3997",
publisher = "Springer New York",
number = "5",

}

TY - JOUR

T1 - RSV causes HIF-1α stabilization via NO release in primary bronchial epithelial cells

AU - Kilani, Muna M.

AU - Mohammed, Kamal A.

AU - Nasreen, Najmunnisa

AU - Tepper, Robert

AU - Antony, Veena B.

PY - 2004/10

Y1 - 2004/10

N2 - 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 VEGF 165. 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.

AB - 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 VEGF 165. 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.

KW - Carboxy-PTIO

KW - ECIS

KW - Edema

KW - VEGF

UR - http://www.scopus.com/inward/record.url?scp=23944496858&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=23944496858&partnerID=8YFLogxK

U2 - 10.1007/s10753-004-6047-y

DO - 10.1007/s10753-004-6047-y

M3 - Article

C2 - 16133997

AN - SCOPUS:23944496858

VL - 28

SP - 245

EP - 251

JO - Inflammation

JF - Inflammation

SN - 0360-3997

IS - 5

ER -