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DOI | 10.1159/000358438 |
Apolipoprotein E-Deficient Mice Are Susceptible to the Development of Acute Lung Injury | |
Yamashita, Cory M.1; Fessler, Michael B.2; Vasanthamohan, Lakshman1; Lac, Joanne1; Madenspacher, Jennifer1; McCaig, Lynda1; Yao, Lijuan1; Wang, Lefeng1; Puntorieri, Valeria1; Mehta, Sanjay1; Lewis, Jim F.1; Veldhuizen, Ruud A. W.1 | |
发表日期 | 2014 |
ISSN | 0025-7931 |
卷号 | 87期号:5页码:416-427 |
英文摘要 | Background: Apolipoprotein E (apoE) has been shown to play a pivotal role in the development of cardiovascular disease, attributable to its function in lipid trafficking and immune modulating properties; however, its role in modulating inflammation in the setting of acute lung injury (ALI) is unknown. Objective: To determine whether apoE-deficient mice (apoE-/-) are more susceptible to ALI compared to wild-type (WT) animals. Methods: Two independent models of ALI were employed. Firstly, WT and apoE-/- mice were randomized to acid aspiration (50 mu l of 0.1 N hydrochloric acid) followed by 4 h of mechanical ventilation. Secondly, WT and apoE-/- mice were randomized to 72 h of hyperoxia exposure or room air. Thereafter, the intrinsic responses of WT and apoE-/- mice were assessed using the isolated perfused mouse lung (IPML) setup. Finally, based on elevated levels of oxidized low-density lipoprotein (oxLDL) in apoE-/-, the effect of oxLDL on lung endothelial permeability and inflammation was assessed. Results: In both in vivo models, apoE-/- mice demonstrated greater increases in lung lavage protein levels, neutrophil counts, and cytokine expression (p < 0.05) compared to WT mice. Experiments utilizing the IPML setup demonstrated no differences in intrinsic lung responses to injury between apoE-/- and WT mice, suggesting the presence of a circulating factor as being responsible for the in vivo observations. Finally, the exposure of lung endothelial cells to oxLDL resulted in increased monolayer permeability and IL-6 release compared to native (nonoxidized) LDL. Conclusions: Our findings demonstrate a susceptibility of apoE-/- animals to ALI that may occur, in part, due to elevated levels of oxLDL. (C) 2014 S. Karger AG, Basel |
英文关键词 | Apolipoprotein E;Acute lung injury;Acid aspiration;Hyperoxia;Oxidized low-density lipoprotein;Gastric acid aspiration |
语种 | 英语 |
WOS记录号 | WOS:000335917000010 |
来源期刊 | RESPIRATION |
来源机构 | 美国环保署 |
文献类型 | 期刊论文 |
条目标识符 | http://gcip.llas.ac.cn/handle/2XKMVOVA/59831 |
作者单位 | 1.Lawson Hlth Res Inst, London, ON, Canada; 2.Natl Inst Environm Hlth Sci, NIH, Res Triangle Pk, NC USA |
推荐引用方式 GB/T 7714 | Yamashita, Cory M.,Fessler, Michael B.,Vasanthamohan, Lakshman,et al. Apolipoprotein E-Deficient Mice Are Susceptible to the Development of Acute Lung Injury[J]. 美国环保署,2014,87(5):416-427. |
APA | Yamashita, Cory M..,Fessler, Michael B..,Vasanthamohan, Lakshman.,Lac, Joanne.,Madenspacher, Jennifer.,...&Veldhuizen, Ruud A. W..(2014).Apolipoprotein E-Deficient Mice Are Susceptible to the Development of Acute Lung Injury.RESPIRATION,87(5),416-427. |
MLA | Yamashita, Cory M.,et al."Apolipoprotein E-Deficient Mice Are Susceptible to the Development of Acute Lung Injury".RESPIRATION 87.5(2014):416-427. |
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