| pubmed-article:19358884 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19358884 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:19358884 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:19358884 | lifeskim:mentions | umls-concept:C1801960 | lld:lifeskim |
| pubmed-article:19358884 | lifeskim:mentions | umls-concept:C2709248 | lld:lifeskim |
| pubmed-article:19358884 | lifeskim:mentions | umls-concept:C0162772 | lld:lifeskim |
| pubmed-article:19358884 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:19358884 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:19358884 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:19358884 | pubmed:dateCreated | 2009-6-2 | lld:pubmed |
| pubmed-article:19358884 | pubmed:abstractText | Acute hypoxia causes pulmonary vascular leak and is involved in the pathogenesis of pulmonary edema associated with inflammation, acute altitude exposure, and other critical illnesses. Reactive oxygen species, HIF-1, and VEGF have all been implicated in various hypoxic pathologies, yet the ROS-HIF-1-VEGF pathway in pulmonary vascular leak has not been defined. We hypothesized that the ROS-HIF-1-VEGF pathway has an important role in producing hypoxia-induced pulmonary vascular leak. Human pulmonary artery endothelial cell (HPAEC) monolayers were exposed to either normoxia (21% O(2)) or acute hypoxia (3% O(2)) for 24 h and monolayer permeability and H(2)O(2), nuclear HIF-1alpha, and cytosolic VEGF levels were determined. HPAEC were treated with antioxidant cocktail (AO; ascorbate, glutathione, and alpha-tocopherol), HIF-1 siRNA, or the VEGF soluble binding protein fms-like tyrosine kinase-1 (sFlt-1) to delineate the role of the ROS-HIF-1-VEGF pathway in hypoxia-induced HPAEC leak. Additionally, mice exposed to hypobaric hypoxia (18,000 ft, 10% O(2)) were treated with the same antioxidant to determine if in vitro responses corresponded to in vivo hypoxia stress. Hypoxia increased albumin permeativity, H(2)O(2) production, and nuclear HIF-1alpha and cytosolic VEGF concentration. Treatment with an AO lowered the hypoxia-induced HPAEC monolayer permeability as well as the elevation of HIF-1alpha and VEGF. Treatment of hypoxia-induced HPAEC with either an siRNA designed against HIF-1alpha or the VEGF antagonist sFlt-1 decreased monolayer permeability. Mice treated with AO and exposed to hypobaric hypoxia (18,000 ft, 10% O(2)) had less pulmonary vascular leak than those that were untreated. Our data suggest that hypoxia-induced permeability is due, in part, to the ROS-HIF-1alpha-VEGF pathway. | lld:pubmed |
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| pubmed-article:19358884 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19358884 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19358884 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19358884 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:19358884 | pubmed:issn | 1873-4596 | lld:pubmed |
| pubmed-article:19358884 | pubmed:author | pubmed-author:MajkaSusanS | lld:pubmed |
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| pubmed-article:19358884 | pubmed:author | pubmed-author:SullivanTimT | lld:pubmed |
| pubmed-article:19358884 | pubmed:author | pubmed-author:IrwinDavid... | lld:pubmed |
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| pubmed-article:19358884 | pubmed:issnType | Electronic | lld:pubmed |
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| pubmed-article:19358884 | pubmed:volume | 47 | lld:pubmed |
| pubmed-article:19358884 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19358884 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19358884 | pubmed:pagination | 55-61 | lld:pubmed |
| pubmed-article:19358884 | pubmed:dateRevised | 2011-10-13 | lld:pubmed |
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| pubmed-article:19358884 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19358884 | pubmed:articleTitle | A potential role for reactive oxygen species and the HIF-1alpha-VEGF pathway in hypoxia-induced pulmonary vascular leak. | lld:pubmed |
| pubmed-article:19358884 | pubmed:affiliation | University of Colorado Health Science Center, School of Medicine, Denver, CO 80262, USA. David.Irwin@ucdenver.edu | lld:pubmed |
| pubmed-article:19358884 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19358884 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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