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Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
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Expression of Niban in renal interstitial fibrosis

Jishi Liu1, Jiao Qin, Wenjuan Mei

  • 1Division of Nephrology, Xiangya Hospital, Central South University, Changsha, China.

Nephrology (Carlton, Vic.)
|April 23, 2014
PubMed
Abstract

Insights

Protein Niban is reduced in renal interstitial fibrosis, and its suppression elevates apoptosis in kidney cells. This suggests Niban plays a role in the development of obstructive nephropathy.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Apoptosis is a key mechanism in renal interstitial fibrosis.
  • Protein Niban's role in tumor cell apoptosis was previously identified.

Purpose of the Study:

  • To assess Niban expression in human and rat renal interstitial fibrosis.
  • To investigate the role of Niban in renal tubular cell apoptosis.

Main Methods:

  • Immunohistochemistry and Western blot for Niban detection.
  • Proteomics and gene array analysis in unilateral-ureteral obstruction (UUO) rat models.
  • TUNEL assay and flow cytometry for apoptosis assessment.
  • siRNA and overexpression studies in HK-2 cells.

Main Results:

  • Niban expression was significantly decreased in renal tubular cells of patients with obstructive nephropathy.
  • Niban levels were reduced in UUO rat kidneys and TGF-β1-stimulated HK-2 cells.
  • siRNA-mediated Niban suppression increased apoptosis in HK-2 cells.

Conclusions:

  • Niban is downregulated in obstructive nephropathy and TGF-β1-induced kidney injury.
  • Niban suppression is linked to increased renal tubular cell apoptosis.
  • Niban may be involved in the pathogenesis of renal interstitial fibrosis.
Keywords:
Chronic Kidney DiseaseNiban (Fam129a)apoptosisrenal interstitial fibrosis

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