NF-κB blockade reduces the O2-evoked rise in Na+ conductance in fetal alveolar cells

John J. E. Haddad; Andrew Collett; Stephen C. Land; Richard E. Olver; Stuart M. Wilson

doi:10.1006/bbrc.2001.4453

NF-κB blockade reduces the O₂-evoked rise in Na⁺ conductance in fetal alveolar cells

John J. E. Haddad, Andrew Collett, Stephen C. Land, Richard E. Olver, Stuart M. Wilson (Lead / Corresponding author)

DArcy Thompson Unit

Research output: Contribution to journal › Article › peer-review

23 Citations (Scopus)

Abstract

Electrophoretic mobility shift assays revealed minimal levels of NF-κB activity in rat distal lung epithelial cells cultured at fetal (23 mmHg) or adult alveolar (100 mmHg) P_O2, but revealed significant activation of this transcription factor in cells exposed to a rise in P_O2 mimicking that experienced at birth. This response was entirely abolished by pretreating cells with 5 mM sulfasalazine (SSA). This shift in P_O2 also evoked a rise in apical Na⁺ conductance (G_Na+) that may underlie the O₂-evoked stimulation of Na⁺ transport seen in these cells. Pretreatment with SSA had no effect upon G_Na+ in cells cultured continually at adult or fetal P_O2 but did inhibit the increase in G_Na+ seen in cells that had experienced the rise in P_O2. O₂-evoked activation of NF-κB may thus mediate the increased Na⁺ transport that occurs when the distal lung epithelial cells are exposed to a physiologically-relevant increase in P_O2.

Original language	English
Pages (from-to)	987-992
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	281
Issue number	4
DOIs	https://doi.org/10.1006/bbrc.2001.4453
Publication status	Published - 9 Mar 2001

Keywords

Alveolar fluid clearance
Epithelial Na channels
Fetal lung
Na transport
NF-κB
Respiratory distress syndrome
Sulfasalazine

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

Access to Document

10.1006/bbrc.2001.4453

Cite this

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title = "NF-κB blockade reduces the O2-evoked rise in Na+ conductance in fetal alveolar cells",

abstract = "Electrophoretic mobility shift assays revealed minimal levels of NF-κB activity in rat distal lung epithelial cells cultured at fetal (23 mmHg) or adult alveolar (100 mmHg) PO2, but revealed significant activation of this transcription factor in cells exposed to a rise in PO2 mimicking that experienced at birth. This response was entirely abolished by pretreating cells with 5 mM sulfasalazine (SSA). This shift in PO2 also evoked a rise in apical Na+ conductance (GNa+) that may underlie the O2-evoked stimulation of Na+ transport seen in these cells. Pretreatment with SSA had no effect upon GNa+ in cells cultured continually at adult or fetal PO2 but did inhibit the increase in GNa+ seen in cells that had experienced the rise in PO2. O2-evoked activation of NF-κB may thus mediate the increased Na+ transport that occurs when the distal lung epithelial cells are exposed to a physiologically-relevant increase in PO2.",

keywords = "Alveolar fluid clearance, Epithelial Na channels, Fetal lung, Na transport, NF-κB, Respiratory distress syndrome, Sulfasalazine",

author = "Haddad, \{John J. E.\} and Andrew Collett and Land, \{Stephen C.\} and Olver, \{Richard E.\} and Wilson, \{Stuart M.\}",

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T1 - NF-κB blockade reduces the O2-evoked rise in Na+ conductance in fetal alveolar cells

AU - Haddad, John J. E.

AU - Collett, Andrew

AU - Land, Stephen C.

AU - Olver, Richard E.

AU - Wilson, Stuart M.

PY - 2001/3/9

Y1 - 2001/3/9

N2 - Electrophoretic mobility shift assays revealed minimal levels of NF-κB activity in rat distal lung epithelial cells cultured at fetal (23 mmHg) or adult alveolar (100 mmHg) PO2, but revealed significant activation of this transcription factor in cells exposed to a rise in PO2 mimicking that experienced at birth. This response was entirely abolished by pretreating cells with 5 mM sulfasalazine (SSA). This shift in PO2 also evoked a rise in apical Na+ conductance (GNa+) that may underlie the O2-evoked stimulation of Na+ transport seen in these cells. Pretreatment with SSA had no effect upon GNa+ in cells cultured continually at adult or fetal PO2 but did inhibit the increase in GNa+ seen in cells that had experienced the rise in PO2. O2-evoked activation of NF-κB may thus mediate the increased Na+ transport that occurs when the distal lung epithelial cells are exposed to a physiologically-relevant increase in PO2.

AB - Electrophoretic mobility shift assays revealed minimal levels of NF-κB activity in rat distal lung epithelial cells cultured at fetal (23 mmHg) or adult alveolar (100 mmHg) PO2, but revealed significant activation of this transcription factor in cells exposed to a rise in PO2 mimicking that experienced at birth. This response was entirely abolished by pretreating cells with 5 mM sulfasalazine (SSA). This shift in PO2 also evoked a rise in apical Na+ conductance (GNa+) that may underlie the O2-evoked stimulation of Na+ transport seen in these cells. Pretreatment with SSA had no effect upon GNa+ in cells cultured continually at adult or fetal PO2 but did inhibit the increase in GNa+ seen in cells that had experienced the rise in PO2. O2-evoked activation of NF-κB may thus mediate the increased Na+ transport that occurs when the distal lung epithelial cells are exposed to a physiologically-relevant increase in PO2.

KW - Alveolar fluid clearance

KW - Epithelial Na channels

KW - Fetal lung

KW - Na transport

KW - NF-κB

KW - Respiratory distress syndrome

KW - Sulfasalazine

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