Tetratricopeptide repeat domain 36 deficiency mitigates renal tubular injury by inhibiting TGF-β1-induced epithelial–mesenchymal transition in a mouse model of chronic kidney disease

Xin Yan; Rui Peng; Yilu Ni; Lei Chen; Qingling He; Qianyin Li; Qin Zhou

doi:10.1016/j.gendis.2021.04.005

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Tetratricopeptide repeat domain 36 deficiency mitigates renal tubular injury by inhibiting TGF-β1-induced epithelial–mesenchymal transition in a mouse model of chronic kidney disease

更新时间：2022-11-09

- Tetratricopeptide repeat domain 36 deficiency mitigates renal tubular injury by inhibiting TGF-β1-induced epithelial–mesenchymal transition in a mouse model of chronic kidney disease
- Genes & Diseases Vol. 9, Issue 6, (2022)
- 作者机构：
  
  The Ministry of Education Key Laboratory of Clinical Diagnostics, School of Laboratory Medicine, Chongqing Medical University,Chongqing,PR China,400016
- 作者简介：
- 基金信息：
- DOI：10.1016/j.gendis.2021.04.005
  CLC：
- Published：2022，
  
  Published Online：1 November 2022，
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Xin Yan, Rui Peng, Yilu Ni, et al. Tetratricopeptide repeat domain 36 deficiency mitigates renal tubular injury by inhibiting TGF-β1-induced epithelial–mesenchymal transition in a mouse model of chronic kidney disease. [J]. Genes & Diseases 9(6).(2022)
DOI：

Xin Yan, Rui Peng, Yilu Ni, et al. Tetratricopeptide repeat domain 36 deficiency mitigates renal tubular injury by inhibiting TGF-β1-induced epithelial–mesenchymal transition in a mouse model of chronic kidney disease. [J]. Genes & Diseases 9(6).(2022) DOI： 10.1016/j.gendis.2021.04.005.

摘要

Abstract

The damage of proximal tubular epithelial cells (PTECs) is considered a central event in the pathogenesis of chronic kidney disease (CKD) and deregulated repair processes of PTECs result in epithelial–mesenchymal transition (EMT)

which in turn aggravates tubular injury and kidney fibrosis. In this study

we firstly revealed that the reduction of TTC36 is associated with unilateral ureteral obstruction (UUO)-induced CKD; besides

ablation of TTC36 attenuated tubular injury and subsequent EMT in UUO-treated mice kidneys. Consistently

TTC36 overexpression promoted EMT in TGF-β1-induced HK2 cells. Moreover

TTC36 elevated the protein expression of CEBPB

which was involved in the regulation of TGF-β/SMAD3 signaling

and augmented SMAD3 signaling and downstream genetic response were reduced by CEBPB silencing. Collectively

our results uncovered that TTC36 deficiency plays a protective role in tubular injury and renal fibrosis triggered by UUO; further

TTC36 overexpression exacerbated TGF-β/SMAD3 signaling via elevating the stability of SMAD3 and CEBPB

suggesting that TTC36 inhibition may be a potential strategy in the therapy of obstructive nephropathy.

关键词

Keywords

CCAAT enhancer binding protein betaChronic kidney diseaseEpithelial−mesenchymal transitionRenal fibrosisSMAD family bember 3Tetratricopeptide repeat domain 36

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