Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2014 Oct 1;327(2):287-96.
doi: 10.1016/j.yexcr.2014.07.001. Epub 2014 Aug 1.

Augmenter of Liver Regeneration Inhibits TGF-β1-induced Renal Tubular Epithelial-To-Mesenchymal Transition via Suppressing TβR II Expression in Vitro

Affiliations

Augmenter of Liver Regeneration Inhibits TGF-β1-induced Renal Tubular Epithelial-To-Mesenchymal Transition via Suppressing TβR II Expression in Vitro

Xiao-Hui Liao et al. Exp Cell Res. .

Abstract

Tubular epithelial-to-mesenchymal transition (EMT) plays a crucial role in the progression of renal tubular interstitial fibrosis (TIF), which subsequently leads to chronic kidney disease (CKD) and eventually, end-stage renal disease (ESRD). We propose that augmenter of liver regeneration (ALR), a member of the newly discovered ALR/Erv1 protein family shown to ameliorate hepatic fibrosis, plays a similar protective role in renal tubular cells and has potential as a new treatment option for CKD. Here, we showed that recombinant human ALR (rhALR) inhibits EMT in renal tubular cells by antagonizing activation of the transforming growth factor-β1 (TGF-β1) signaling pathway. Further investigation revealed that rhALR suppresses the expression of TGF-β receptor type II (TβR II) and significantly alleviates TGF-β1-induced phosphorylation of Smad2 and nuclear factor-κB (NF-κB). No apparent adverse effects were observed upon the addition of rhALR alone to cells. These findings collectively suggest that ALR plays a role in inhibiting progression of renal tubular EMT, supporting its potential utility as an effective antifibrotic strategy to reverse TIF in CKD.

Keywords: Augmenter of liver regeneration; Renal tubular epithelial cells; TGFβR II; Transforming growth factor-β1; Tubular epithelial-to-mesenchymal transition.

Similar articles

See all similar articles

Cited by 3 articles

Publication types

MeSH terms

Substances

LinkOut - more resources

Feedback