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Hypoxic activation of an amiloride-sensitive cation conductance in alveolar epithelial cells.
- Source :
-
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2001 Aug 24; Vol. 286 (3), pp. 622-7. - Publication Year :
- 2001
-
Abstract
- Imposing hypoxia (P(O(2)) = 23 mmHg) upon A549 cells elicited increased G(amil) although previous work had predicted a fall in this parameter. G(amil) appeared to be dependent upon glucocorticoid-driven gene expression, a process inhibited by ERK, an enzyme activated by oxidative stress. However, hypoxia transiently activated this enzyme and the response was blocked by glucocorticoids, showing that the rise in G(amil) occurs only if ERK activation is suppressed. Fluorimetric assays showed that lowering P(O(2)) elicited H(2)O(2) formation indicating that this maneuver actually imposes oxidative stress, thus explaining how hypoxia can elicit responses normally associated with a rise in P(O(2)).<br /> (Copyright 2001 Academic Press.)
- Subjects :
- Animals
Cell Hypoxia
Cell Line
Dexamethasone pharmacology
Electric Conductivity
Glucocorticoids pharmacology
Hormone Antagonists pharmacology
Hydrogen Peroxide metabolism
Ion Transport
Mifepristone pharmacology
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinases antagonists & inhibitors
Mitogen-Activated Protein Kinases metabolism
Oxidative Stress
Oxygen physiology
Pressure
Respiratory Mucosa drug effects
Amiloride pharmacology
Pulmonary Alveoli cytology
Respiratory Mucosa physiology
Sodium metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0006-291X
- Volume :
- 286
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Biochemical and biophysical research communications
- Publication Type :
- Academic Journal
- Accession number :
- 11511105
- Full Text :
- https://doi.org/10.1006/bbrc.2001.5432