Advanced Glycation Endproducts Stimulate Renal Epithelial Cells to Release Chemokines That Recruit Macrophages, Leading to Renal Fibrosis
Advanced Glycation Endproducts Stimulate Renal Epithelial Cells to Release Chemokines That Recruit Macrophages, Leading to Renal Fibrosis
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DOI：
10.1271/bbb.120347
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发表时间：
2012-09
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影响因子：
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通讯作者：
Yosuke Sasai;Kousei Iwakawa;Kanako Yanagida;Yan Shen;Takashi Hosono;T. Ariga;T. Seki
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文献类型：
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作者：
Yosuke Sasai;Kousei Iwakawa;Kanako Yanagida;Yan Shen;Takashi Hosono;T. Ariga;T. Seki
糖尿病肾病是糖尿病的主要并发症，肾小管间质纤维化是其主要表现之一。本研究旨在阐明晚期糖基化终产物（AGEs）对肾小管上皮细胞株NRK-52 E的致病性。AGE暴露的细胞显着增加了转化生长因子β，纤溶酶原激活物抑制剂-1，和组织转氨酶的基因表达，并由他们的条件培养基显示出强大的潜力，招募巨噬细胞，部分通过趋化因子，单核细胞趋化蛋白-1。在37 °C下保持120 d变性的白蛋白具有相似的活性，但低于AGEs。因此，在糖尿病患者中产生的AGEs可能直接通过肾上皮细胞刺激和间接通过巨噬细胞募集来加剧肾脏中的纤维化。
Diabetic nephropathy is a major complication of diabetes and tubulointerstitial fibrosis is one of its manifestations. This study aimed to clarify the pathogenicity of advanced glycation endproducts (AGEs) toward NRK-52E, a tubular epithelial cell line. The AGE-exposed cells significantly increased gene expression of transforming growth factor beta, plasminogen activator inhibitor-1, and tissue transglutaminase, and a medium conditioned by them showed strong potential to recruit macrophages, partly through a chemokine, monocyte chemoattractant protein-1. Albumin denatured by maintenance at 37 °C for 120 d exhibited similar activities, but they were lower than those of the AGEs. Thus, AGEs generated in diabetic patients might exacerbate fibrosis in the kidneys directly through renal epithelial cell stimulation, and indirectly by recruitment of macrophages.