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Advanced glycation end-products and receptor for advanced glycation end-products expression in patients with idiopathic pulmonary fibrosis and NSIP

Authors
Kyung, Sun YoungByun, Kyung HeeYoon, Jin YoungKim, Yu JinLee, Sang PyoPark, Jeong-WoongLee, Bong HeePark, Jong SookJang, An SooPark, Choon SikJeong, Sung Hwan
Issue Date
2014
Publisher
e-Century Publishing Corporation
Keywords
Advanced glycation end products; Idiopathic pulmonary fibrosis; receptor for advanced glycation end product
Citation
International Journal of Clinical and Experimental Pathology, v.7, no.1, pp 221 - 228
Pages
8
Journal Title
International Journal of Clinical and Experimental Pathology
Volume
7
Number
1
Start Page
221
End Page
228
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/13033
ISSN
1936-2625
Abstract
Advanced glycation end products (AGEs) are associated with the pathogenesis of various diseases. AGEs induce excess accumulation of extracellular matrix and expression of profibrotic cytokines. In addition, studies on receptor for advanced glycation end products (RAGE) have shown that the ligand-RAGE interaction activates several intracellular signaling cascades associated with several fibrotic diseases. We investigated the expression of AGEs and RAGE in samples from patients with idiopathic pulmonary fibrosis (IPF) and nonspecific interstitial pneumonia (NSIP). Lung tissues and plasma samples from patients with IPF (n=10), NSIP (n=10), and control subjects (n=10) were obtained. Expression of AGEs and RAGE was determined by immunofluorescence assay of lung tissue. Circulating AGEs were measured by Western blot and enzyme-linked immunosorbent assay. Lungs with IPF showed strong expression for both AGEs and RAGE compared to that in NSIP and controls. However, no difference in AGE or RAGE expression was observed in lungs with NSIP compared to that in the controls. Levels of circulating AGEs also increased significantly in lungs of patients with IPF compared to those with NSIP and normal control. Increased AGE-RAGE interaction may play an important role in the pathogenesis of IPF.
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