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Receptor for advanced glycation end-products is a marker of type I cell injury in acute lung injury.
TLDR
RAGE is a marker of type I alveolar epithelial epithelial cell injury based on experimental studies in rats and in patients with acute lung injury. Expand
Prolonged hypoxia differentially regulates hypoxia-inducible factor (HIF)-1alpha and HIF-2alpha expression in lung epithelial cells: implication of natural antisense HIF-1alpha.
TLDR
Data indicate that, during prolonged hypoxia, HIF-alpha proteins negatively regulate Hif-1alpha expression through an increase in aHIF and destabilization of HIF -1alpha mRNA, likely conveys target gene specificity. Expand
Activation of the alpha7 nAChR reduces acid-induced acute lung injury in mice and rats.
TLDR
Results indicate that activation of alpha7 nAChR may provide a new therapeutic pathway for the treatment of acute lung injury. Expand
Prolonged Hypoxia Differentially Regulates Hypoxia-inducible Factor (HIF)-1α and HIF-2α Expression in Lung Epithelial Cells
TLDR
Data indicate that, during prolonged hypoxia, HIF-α proteins negatively regulate Hif-1α expression through an increase in aHIF and destabilization of HIF/2α mRNA, which likely conveys target gene specificity. Expand
Hypoxia upregulates VEGF expression in alveolar epithelial cells in vitro and in vivo.
TLDR
Findings suggest that release of VEGF synthesized by AEC may target not only endothelial cells but also other alveolar cells, including macrophages and epithelial cells, as well as bronchoalveolar lavage fluid. Expand
Activation of the α7 nAChR Reduces Acid-Induced Acute Lung Injury in Mice and Rats
TLDR
It is found that nicotine, choline, and PNU-282987 (a specific α7 nAChR agonist) decreased excess lung water and lung vascular permeability, and reduced protein concentration in the bronchoalveolar lavage (BAL). Expand
Hypoxia and beta 2-agonists regulate cell surface expression of the epithelial sodium channel in native alveolar epithelial cells.
TLDR
It is established that hypoxia-induced inhibition of amiloride-sensitive sodium channel activity is mediated by decreased apical expression of ENaC subunits and that beta(2)-agonists reverse this effect by enhancing the insertion of ENc subunits into the membrane of hypoxic alveolar epithelial cells. Expand
Elevated levels of the receptor for advanced glycation end products, a marker of alveolar epithelial type I cell injury, predict impaired alveolar fluid clearance in isolated perfused human lungs.
TLDR
RAGE may be a useful biological marker of alveolar epithelial injury and impaired AFC in donor lungs prior to transplant and perhaps in patients with acute lung injury. Expand
Physiological and biochemical markers of alveolar epithelial barrier dysfunction in perfused human lungs.
TLDR
Data show that preserved AFC is a critical determinant of favorable lung fluid balance in the perfused human lung, raising the possibility that beta(2)-agonist therapy to increase edema fluid clearance may be of value for patients with acute lung injury and pulmonary edema. Expand
Hypoxia and β2-Agonists Regulate Cell Surface Expression of the Epithelial Sodium Channel in Native Alveolar Epithelial Cells*
TLDR
It is established that hypoxia-induced inhibition of amiloride-sensitive sodium channel activity is mediated by decreased apical expression of ENaC subunits and that β2-agonists reverse this effect by enhancing the insertion of ENc subunits into the membrane of hypoxic alveolar epithelial cells. Expand
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