Phosphotriesterase-related protein sensed albuminuria and conferred renal tubular cell activation in membranous nephropathy

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• 作者：Chao-Wen Cheng (1) (2) (3)
  Li-Chien Chang (4)
  Tzu-Ling Tseng (5)
  Chia-Chao Wu (6)
  Yuh-Feng Lin (1) (7)
  Jin-Shuen Chen (6)
  
  1. Graduate Institute of Clinical Medicine ; College of Medicine ; Taipei Medical University ; Taipei ; Taiwan
  2. Center for Translational Medicine ; College of Medical Science and Technology ; Taipei Medical University ; Taipei ; Taiwan
  3. Graduate Institute of Medical Sciences ; Taipei ; Taiwan
  4. School of Pharmacy ; National Defense Medical Center ; Taipei ; Taiwan
  5. Biomedical Technology & Device Research Laboratories ; Industrial Technology Research Institute ; Hsinchu ; Taiwan
  6. Division of Nephrology ; Department of Internal Medicine ; Tri-Service General Hospital ; 325 ; Sec. 2 ; Cheng-Kung Rd. ; Neihu 114 Taipei ; Taiwan ; Republic of China
  7. Department of Internal Medicine ; Shuang Ho Hospital ; Taipei Medical University ; New Taipei ; Taiwan
  
• 关键词：Albuminuria ; Nephrotic syndrome ; Phosphotriesterase ; related protein (PTER)
• 刊名：Journal of Biomedical Science
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：21
• 期：1
• 全文大小：894 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Biomedicine
  
• 出版者：Springer Netherlands
• ISSN：1423-0127

文摘

Background Membranous nephropathy (MN) is a common cause of nephrotic syndrome that may progress to end-stage renal disease (ESRD). The formation of MN involves the in situ formation of subepithelial immune deposits and leads to albuminuria; however, the underlying mechanism of how MN leads to ESRD remains unclear. The aim of this study was to investigate the expression and biological functions of phosphotriesterase-related protein (PTER) in MN. Results In the progression of MN, the expression of PTER increased significantly and was mainly expressed in the renal tubular cells. Both mRNA and protein expression levels of PTER were increased in a concentration- and time-dependent manner in the in vitro albuminuria tubular cell model. Silencing the expression of PTER by RNA interference diminished albuminuria-induced inflammatory and pro-fibrotic cytokines production. Conclusions Our findings reveal that PTER may sense albuminuria in the progression of MN, induce tubular cell activation and lead to ESRD.