| Receptor for advanced glycation end-products (RAGE) is an indicator of direct lung injury in models of experimental lung injury. | |
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MedLine Citation:
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PMID: 19411309 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Receptor for advanced glycation end-products (RAGE) is a marker of alveolar type I cells and is elevated in the pulmonary edema fluid of patients with acute lung injury (ALI). We tested the hypothesis that RAGE in the bronchoalveolar lavage (BAL) would be elevated in experimental models of direct ALI characterized by alveolar epithelial cell injury. We developed ELISA measurements for RAGE and studied ALI (direct and indirect) mouse models and collected BAL at specified endpoints to measure RAGE. We also tested whether levels of BAL RAGE correlated 1) with the severity of lung injury in acid and hyperoxia-induced ALI and 2) with the beneficial effect of a novel treatment, mesenchymal stem cells (MSC), in LPS-induced ALI. In ALI models of direct lung injury induced by intratracheal instillation of acid, LPS, or Escherichia coli, the BAL RAGE was 58-, 22-, and 13-fold elevated, respectively. In contrast, BAL RAGE was not detectable in indirect models of ALI induced by an intraperitoneal injection of thiourea or by an intravenous injection of MHC I monoclonal antibody that produces a mouse model of transfusion-related ALI. BAL RAGE did correlate with the severity of lung injury in acid and hyperoxia-induced ALI. In addition, with LPS-induced ALI, BAL RAGE was markedly reduced with MSC treatment. In summary, BAL RAGE is an indicator of ALI, and it may be useful in distinguishing direct from indirect models of ALI as well as assessing the response to specific therapies. |
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Authors:
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Xiao Su; Mark R Looney; Naveen Gupta; Michael A Matthay |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-05-01 |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 297 ISSN: 1522-1504 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2009 Jul |
Date Detail:
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Created Date: 2009-06-29 Completed Date: 2009-08-11 Revised Date: 2010-09-24 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L1-5 Citation Subset: IM |
Affiliation:
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Cardiovascular Research Institute, University of California, San Francisco, California 94143-0130, USA. suxiao1@yahoo.com |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acids Acute Lung Injury / chemically induced*, metabolism*, pathology, therapy Animals Bronchoalveolar Lavage Fluid / cytology Cell Count Disease Models, Animal Hydrogen-Ion Concentration Hyperoxia / complications Lipopolysaccharides Mesenchymal Stem Cells / cytology Mice Mice, Inbred C57BL Neutrophils / cytology Receptors, Immunologic / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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HL-081027/HL/NHLBI NIH HHS; HL-082742/HL/NHLBI NIH HHS; HL-51854/HL/NHLBI NIH HHS; HL-51856/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Acids; 0/Lipopolysaccharides; 0/Receptors, Immunologic; 0/advanced glycosylation end-product receptor |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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