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学科主题: 临床医学
题名:
Kidney injury molecule-1 expression in IgA nephropathy and its correlation with hypoxia and tubulointerstitial inflammation
作者: Lin, Qiongzhen1,2,3; Chen, Ying1,2,3; Lv, Jicheng1,2,3; Zhang, Hong1,2,3; Tang, Jiawei1,2,3; Gunaratnam, Lakshman4; Li, Xiaomei1,2,3; Yang, Li1,2,3
关键词: kidney injury molecule-1 ; IgA nephropathy ; hypoxia ; tubulointerstitial inflammation
刊名: AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
发表日期: 2014-04-01
DOI: 10.1152/ajprenal.00331.2013
卷: 306, 期:8, 页:F885-F895
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Physiology ; Urology & Nephrology
研究领域[WOS]: Physiology ; Urology & Nephrology
关键词[WOS]: MONOCYTE CHEMOATTRACTANT PROTEIN-1 ; TUBULAR EPITHELIAL-CELLS ; MURINE PERITONEAL-MACROPHAGES ; STAGE RENAL-FAILURE ; DIABETIC-NEPHROPATHY ; URINARY BIOMARKER ; IN-VITRO ; DISEASE ; KIM-1 ; MECHANISMS
英文摘要:

Tubulointerstitial injury plays an important role in the development and progression of chronic kidney disease (CKD). Kidney injury molecule (KIM)-1 is induced in damaged proximal tubules in both acute renal injury and CKD. However, the dynamics of KIM-1 in CKD and effects of KIM-1 expression on disease progression are unknown. Here, we aimed to determine the associations between tubular KIM-1 expression levels, renal function, and inflammation in CKD. The relationships between levels of KIM-1 and clinicopathological parameters were analyzed in patients with progressive and nonprogressive IgA nephropathy. KIM-1 expression was increased in patients with IgA nephropathy, and its expression was significantly correlated with the decrease of renal function. KIM-1 was particularly evident at the site with reduced capillary density, and KIM-1-positive tubules were surrounded by infiltrates of inflammatory cells. Using in vitro cell models, we showed that cellular stressors, including hypoxia, induced KIM-1 expression. KIM-1-expressing cells produced more chemokines/cytokines when cultured under hypoxic conditions. Furthermore, we showed that tubular cells with KIM-1 expression can regulate the immune response of inflammatory cells through the secretion of chemotactic factors. These data suggest that KIM-1-expressing epithelial cells may play a role in the pathogenesis of tubulointerstitial inflammation during chronic renal injury through the secretion of chemokines/cytokines.

语种: 英语
所属项目编号: 81070549 ; 81270777
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000334610000010
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57306
Appears in Collections:北京大学第一临床医学院_肾脏内科_期刊论文

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作者单位: 1.Minist Hlth China, Key Lab Renal Dis, Beijing, Peoples R China
2.Peking Univ, Hosp 1, Dept Med, Div Renal, Beijing 100034, Peoples R China
3.Peking Univ, Inst Nephrol, Beijing 100034, Peoples R China
4.Univ Western Ontario, Dept Med, Dept Microbiol & Immunol, London, ON, Canada

Recommended Citation:
Lin, Qiongzhen,Chen, Ying,Lv, Jicheng,et al. Kidney injury molecule-1 expression in IgA nephropathy and its correlation with hypoxia and tubulointerstitial inflammation[J]. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY,2014,306(8):F885-F895.
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