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

Chao Wen Cheng, Li Chien Chang, Tzu Ling Tseng, Chia Chao Wu, Yuh Feng Lin, Jin Shuen Chen

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number32
JournalJournal of Biomedical Science
Volume21
Issue number1
DOIs
Publication statusPublished - Apr 22 2014

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Phosphoric Triester Hydrolases
Membranous Glomerulonephritis
Albuminuria
Chemical activation
Kidney
Chronic Kidney Failure
Proteins
Nephrotic Syndrome
RNA Interference
Deposits
RNA
Cytokines
Messenger RNA

Keywords

  • Albuminuria
  • Nephrotic syndrome
  • Phosphotriesterase-related protein (PTER)

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Molecular Biology
  • Cell Biology
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism
  • Pharmacology (medical)

Cite this

Phosphotriesterase-related protein sensed albuminuria and conferred renal tubular cell activation in membranous nephropathy. / Cheng, Chao Wen; Chang, Li Chien; Tseng, Tzu Ling; Wu, Chia Chao; Lin, Yuh Feng; Chen, Jin Shuen.

In: Journal of Biomedical Science, Vol. 21, No. 1, 32, 22.04.2014.

Research output: Contribution to journalArticle

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AU - Cheng, Chao Wen

AU - Chang, Li Chien

AU - Tseng, Tzu Ling

AU - Wu, Chia Chao

AU - Lin, Yuh Feng

AU - Chen, Jin Shuen

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N2 - 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.

AB - 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.

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