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Adrenomedullin expression in a rat model of acute lung injury induced by hypoxia and LPS
Authors: Agorreta, J. (Jackeline)
Zulueta, J.J. (Javier J.)
Montuenga, L.M. (Luis M.)
Garayoa, M. (Mercedes)
Keywords: Acute respiratory distress syndrome
Endotoxin
Alveolar macrophages
Endothelial cells
Type II pneumocytes
Issue Date: 2005
Publisher: American Physiological Society
Publisher version: http://dx.doi.org/10.1152/ajplung.00314.2004
ISSN: 1040-0605
Citation: Agorreta J, Zulueta JJ, Montuenga LM, Garayoa M. Adrenomedullin expression in a rat model of acute lung injury induced by hypoxia and LPS. Am J Physiol Lung Cell Mol Physiol 2005 Mar;288(3):L536-L545.
Abstract
Adrenomedullin (ADM) is upregulated independently by hypoxia and LPS, two key factors in the pathogenesis of acute lung injury (ALI). This study evaluates the expression of ADM in ALI using experimental models combining both stimuli: an in vivo model of rats treated with LPS and acute normobaric hypoxia (9% O2) and an in vitro model of rat lung cell lines cultured with LPS and exposed to hypoxia (1% O2). ADM expression was analyzed by in situ hybridization, Northern blot, Western blot, and RIA analyses. In the rat lung, combination of hypoxia and LPS treatments overcomes ADM induction occurring after each treatment alone. With in situ techniques, the synergistic effect of both stimuli mainly correlates with ADM expression in inflammatory cells within blood vessels and, to a lesser extent, to cells in the lung parenchyma and bronchiolar epithelial cells. In the in vitro model, hypoxia and hypoxia LPS treatments caused a similar strong induction of ADM expression and secretion in epithelial and endothelial cell lines. In alveolar macrophages, however, LPS-induced ADM expression and secretion were further increased by the concomitant exposure to hypoxia, thus paralleling the in vivo response. In conclusion, ADM expression is highly induced in a variety of key lung cell types in this rat model of ALI by combination of hypoxia and LPS, suggesting an essential role for this mediator in this syndrome
Permanent link: http://hdl.handle.net/10171/16769
Appears in Collections:DA - Ciencias - HAP - Artículos de revista
DA - CIMA - Oncología - Biomarcadores - Artículos de Revista

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