Advanced glycation end-products and receptor for advanced glycation end-products expression in patients with idiopathic pulmonary fibrosis and NSIP.
Advanced glycation end-products and receptor for advanced glycation end-products expression in patients with idiopathic pulmonary fibrosis and NSIP.
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发表时间：
2014
影响因子：
1.4
通讯作者：
S. Kyung;K. Byun;J. Y. Yoon;Y. J. Kim;S. Lee;Jeong-Woong Park;Bong-Hee Lee;Jong Sook Park;A. Jang;Choon-Sik Park;S. Jeong
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作者：
S. Kyung;K. Byun;J. Y. Yoon;Y. J. Kim;S. Lee;Jeong-Woong Park;Bong-Hee Lee;Jong Sook Park;A. Jang;Choon-Sik Park;S. Jeong
糖基化终末产物（AGEs）与多种疾病的发生、发展密切相关。AGEs诱导细胞外基质的过度积累和促纤维化细胞因子的表达。此外，对晚期糖基化终末产物受体（receptor for advanced glycation end products，RECEPTOR）的研究表明，配体-受体相互作用激活了与多种纤维化疾病相关的几种细胞内信号级联。我们研究了特发性肺纤维化（IPF）和非特异性间质性肺炎（NSIP）患者样本中AGEs和AGEs的表达。获得IPF患者（n=10）、NSIP患者（n=10）和对照受试者（n=10）的肺组织和血浆样本。采用免疫荧光法检测肺组织AGEs和TGF β 1的表达。采用Western blot和酶联免疫吸附试验检测循环AGEs。与NSIP和对照组相比，IPF肺组织中AGEs和TGF-β的表达均较强。然而，与对照组相比，在NSIP肺中未观察到AGE或ESTmRNA表达的差异。与NSIP和正常对照组相比，IPF患者肺中循环AGEs水平也显著升高。AGE-CRP相互作用增加可能在IPF发病机制中发挥重要作用。
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 non-specific 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.