Abstract
Renal fibrosis is a hallmark in CKD (chronic kidney disease) and is strongly correlated to the deterioration of renal function that is characterized by tubulointerstitial fibrosis, tubular atrophy, glomerulosclerosis and disruption of the normal architecture of the kidney. ALR (augmenter of liver regeneration) is a growth factor with biological functions similar to those of HGF (hepatocyte growth factor). In this study, our results indicate that endogenous ALR is involved in the pathological progression of renal fibrosis in UUO (unilateral ureteral obstruction) rat model. Moreover, we find that administration of rhALR (recombinant human ALR) significantly alleviates renal interstitial fibrosis and reduces renal-fibrosis-related proteins in UUO rats. Further investigation reveals that rhALR suppresses the up-regulated expression of TGF-β1 (transforming growth factor β1) induced by UUO operation in the obstructed kidney, and inhibits Smad2 and Smad3 phosphorylation activated by the UUO-induced injury in the animal model. Therefore we suggest that ALR is involved in the progression of renal fibrosis and administration of rhALR protects the kidney against renal fibrosis by inhibition of TGF-β/Smad activity.
Highlights
chronic kidney disease (CKD) has received increasing attention as a leading public health problem with rapid growth in its prevalence
Effects of rats. The exogenous ALR (rhALR) on the proteins involved in renal fibrosis in rat UUO model We investigated the expression of proteins related to renal fibrosis, such as E-cadherin, vimentin, α-SMA, fibronectin and collagen I in PBS- or rhALR-treated rat UUO kidneys
We investigated the effects of rhALR on the renal tubulointerstitial fibrosis induced by UUO in rats
Summary
CKD (chronic kidney disease) has received increasing attention as a leading public health problem with rapid growth in its prevalence. Renal fibrosis is a pathological hallmark of CKD, which is characterized by tubulointerstitial fibrosis, tubular atrophy, glomerulosclerosis and disruption of the normal architecture of the kidney It strongly correlates with the deterioration of the renal function, and leads to ESRD (end-stage renal disease) [3]. Numerous studies have shown that the progressive renal fibrosis is mediated by the growth factors, cytokines, metabolic toxins and stress molecules via complex mechanisms and multiple pathways. Among these mediators, TGF-β1 (transforming growth factor β1) has been recognized as a key promoter in the pathogenesis of renal fibrosis [6,7,8].
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