期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 304, 期 4, 页码 L250-L263出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00278.2012
关键词
receptor for advanced glycation end products; red blood cell transfusion; endothelial cell; lung inflammation; red blood cells
资金
- National Heart, Lung, and Blood Institute [HL-098362]
- National Blood Foundation
- American Lung Association
Mangalmurti NS, Friedman JL, Wang L, Stolz D, Muthukumaran G, Siegel DL, Schmidt AM, Lee JS, Albelda SM. The receptor for advanced glycation end products mediates lung endothelial activation by RBCs. Am J Physiol Lung Cell Mol Physiol 304: L250-L263, 2013. First published December 28, 2012; doi:10.1152/ajplung.00278.2012.-The receptor for advanced glycation end products (RAGE) is a multiligand pattern recognition receptor implicated in multiple disease states. Although RAGE is expressed on systemic vascular endothelium, the expression and function of RAGE on lung endothelium has not been studied. Utilizing in vitro (human) and in vivo (mouse) models, we established the presence of RAGE on lung endothelium. Because RAGE ligands can induce the expression of RAGE and stored red blood cells express the RAGE ligand N-epsilon-carboxymethyl lysine, we investigated whether red blood cell (RBC) transfusion would augment RAGE expression on endothelium utilizing a syngeneic model of RBC transfusion. RBC transfusion not only increased lung endothelial RAGE expression but enhanced lung inflammation and endothelial activation, since lung high mobility group box 1 and vascular cell adhesion molecule 1 expression was elevated following transfusion. These effects were mediated by RAGE, since endothelial activation was absent in RBC-transfused RAGE knockout mice. Thus, RAGE is inducibly expressed on lung endothelium, and one functional consequence of RBC transfusion is increased RAGE expression and endothelial activation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据