Hyperbaric oxygenation upregulates rat lung Na,K-ATPase

Harris, Z. Leah; Ridge, KM; González-Flecha, Beatriz; Gottlieb, Lawrence J.; Zucker, Anna; Sznajder, J. I.

doi:10.1183/09031936.96.09030472

Cited by 19 publications

(9 citation statements)

References 21 publications

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“…It is well established that oxidant-induced lung injury results in damage of the alveolar capillary barrier causing capillary leak and lung edema accumulation. Previous studies show that this process results in upregulation of pulmonary Na,K-ATPase as a part of the protective mechanism against reactive oxygen species [12][13][14][15]. Our results are consistent with these findings showing a hyperoxic-induced lung edema formation and increased nonselective permeability of alveolar epithelium as well as upregulation of Na,KATPase gene expression.…”

Section: Discussionsupporting

confidence: 82%

“…These events may lead to upregulation of pulmonary Na,K-ATPase and increase sodium clearance across the alveolar epithelium as a part of the protective mechanism against reactive oxygen species generated during hyperoxia [12][13][14][15]. In some cases reactive oxygen species, such as super oxide anion, hydroxyl radical and hydrogen peroxide, may be generated at a rate that overwhelms the natural defenses of the cell leading to destructive oxidation [16].…”

Section: Introductionmentioning

confidence: 99%

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Influence of Inhaled Nitric Oxide and Hyperoxia on Na,K-ATPase Expression and Lung Edema in Newborn Piglets

Youssef¹,

Thibeault²,

Rezaiekhaligh³

et al. 1999

Neonatology

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This study was undertaken to examine the combined effect of nitric oxide (NO) and hyperoxia on lung edema and Na,K-ATPase expression. Newborn piglets were exposed to room air (FiO₂ = 0.21), room air plus 50 ppm NO, hyperoxia (FiO₂ ≥ 0.96) or to hyperoxia plus 50 ppm NO for 4–5 days. Animals exposed to NO in room air experienced only a slight decrease in Na,K-ATPase α subunit protein level. Hyperoxia, in the absence of NO, induced both the mRNA and the protein level of Na,K-ATP-ase α subunit and significantly increased wet lung weight, extravascular lung water, and alveolar permeability. NO in hyperoxia decreased the hyperoxic-mediated induction of Na,K-ATPase α subunit mRNA and protein while wet lung weight, extravascular lung water, and alveolar permeability remained elevated. These results suggest that 50 ppm of inhaled NO may not improve hyperoxic-induced lung injury and may interfere with the expression of Na,K-ATPase which constitutes a part of the cellular defense mechanism against oxygen toxicity.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Influence of Inhaled Nitric Oxide and Hyperoxia on Na,K-ATPase Expression and Lung Edema in Newborn Piglets

Youssef¹,

Thibeault²,

Rezaiekhaligh³

et al. 1999

Neonatology

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“…Exposure of rats to sublethal hyperoxia (85% O 2 ) increased alveolar type II cell ␣-rENaC mRNA level (387). In addition, it has been recently reported that ␣ 1 -and ␤ 1 -Na ϩ -K ϩ -ATPase mRNA subunit levels both increased in alveolar type II cells from rats exposed to hyperoxia (148). The mechanism whereby O 2 tension regulates sodium channels and Na ϩ -K ϩ -ATPase gene expression is thought to be transcriptional.…”

Section: B Hypoxiamentioning

confidence: 99%

Lung Epithelial Fluid Transport and the Resolution of Pulmonary Edema

Matthay

Folkesson²,

Clérici³

2002

Physiological Reviews

612

649

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The discovery of mechanisms that regulate salt and water transport by the alveolar and distal airway epithelium of the lung has generated new insights into the regulation of lung fluid balance under both normal and pathological conditions. There is convincing evidence that active sodium and chloride transporters are expressed in the distal lung epithelium and are responsible for the ability of the lung to remove alveolar fluid at the time of birth as well as in the mature lung when pathological conditions lead to the development of pulmonary edema. Currently, the best described molecular transporters are the epithelial sodium channel, the cystic fibrosis transmembrane conductance regulator, Na+-K+-ATPase, and several aquaporin water channels. Both catecholamine-dependent and -independent mechanisms can upregulate isosmolar fluid transport across the distal lung epithelium. Experimental and clinical studies have made it possible to examine the role of these transporters in the resolution of pulmonary edema.

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“…Transcription factors are also involved in sodium pump gene regulation as was observed in renal cells undergoing hypoxia where ␤ 1 transcription was enhanced by the binding of SP1/SP3 near the promoter region of ␤ 1 (25,26). The up-or downregulation of sodium pump expression and activity plays a role in preventing the exacerbation of some diseases as is the case during hyperbaric oxygenation of the lung where increased ␣ 1 and ␤ 1 subunit levels help to prevent pulmonary edema (27). In renal carcinoma-like cells, the increased expression of heterologous sodium pump ␤ 1 subunits reduces cell motility and invasiveness by forming intercellular interactions between adjacent ␤ subunits (28,29).…”

mentioning

confidence: 99%

Regulation of Na,K-ATPase Subunit Abundance by Translational Repression

Clifford

Kaplan

2009

Journal of Biological Chemistry

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The Na,K-ATPase is an ␣␤ heterodimer responsible for maintaining fluid and electrolyte homeostasis in mammalian cells. We engineered Madin-Darby canine kidney cell lines expressing ␣ 1 FLAG, ␤ 1 FLAG, or ␤ 2 MYC subunits via a tetracycline-regulated promoter and a line expressing both stable ␤ 1 MYC and tetracycline-regulated ␤ 1 FLAG to examine regulatory mechanisms of sodium pump subunit expression. When overexpression of exogenous ␤ 1 FLAG increased total ␤ subunit levels by >200% without changes in ␣ subunit abundance, endogenous ␤ 1 subunit (␤ 1 E) abundance decreased. ␤ 1 E downregulation did not occur during ␤ 2 MYC overexpression, indicating isoform specificity of the repression mechanism. Measurements of RNA stability and content indicated that decreased ␤ subunit expression was not accompanied by any change in mRNA levels. In addition, the degradation rate of ␤ subunits was not altered by ␤ 1 FLAG overexpression. Cells stably expressing ␤ 1 MYC, when induced to express ␤ 1 FLAG subunits, showed reduced ␤ 1 MYC and ␤ 1 E subunit abundance, indicating that these effects occur via the coding sequences of the down-regulated polypeptides. In a similar way, Madin-Darby canine kidney cells overexpressing exogenous ␣ 1 FLAG subunits exhibited a reduction of endogenous ␣ 1 subunits (␣ 1 E) with no change in ␣ mRNA levels or ␤ subunits. The reduction in ␣ 1 E compensated for ␣ 1 FLAG subunit expression, resulting in unchanged total ␣ subunit abundance. Thus, regulation of ␣ subunit expression maintained its native level, whereas ␤ subunit was not as tightly regulated and its abundance could increase substantially over native levels. These effects also occurred in human embryonic kidney cells. These data are the first indication that cellular sodium pump subunit abundance is modulated by translational repression. This mechanism represents a novel, potentially important mechanism for regulation of Na,K-ATPase expression.

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Hyperbaric oxygenation upregulates rat lung Na,K-ATPase

Cited by 19 publications

References 21 publications

Influence of Inhaled Nitric Oxide and Hyperoxia on Na,K-ATPase Expression and Lung Edema in Newborn Piglets

Influence of Inhaled Nitric Oxide and Hyperoxia on Na,K-ATPase Expression and Lung Edema in Newborn Piglets

Lung Epithelial Fluid Transport and the Resolution of Pulmonary Edema

Regulation of Na,K-ATPase Subunit Abundance by Translational Repression

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