| Literature DB >> 26616407 |
Zhihui Yao1,2, Sisi Yang1,2, Weifeng He1,2, Lian Li1,3, Rui Xu1, Xiaorong Zhang1, Haisheng Li1, Rixing Zhan1, Wei Sun1, Jianglin Tan1, Junyi Zhou1, Gaoxing Luo1,2, Jun Wu1,2.
Abstract
P311, a gene that was identified in 1993, has been found to have diverse biological functions in processes such as cell proliferation, migration and differentiation. However, its role in fibrosis is unknown. We previously observed that P311 is highly expressed in skin hypertrophic scars. In this study, P311 over-expression was detected in a subset of tubular epithelial cells in clinical biopsy specimens of renal fibrosis; this over-expression, was found concurrent with α-smooth muscle actin (α-SMA) and transforming growth factor beta1 (TGFβ1) expression. Subsequently, these results were verified in a mouse experimental renal fibrosis model induced by unilateral ureteral obstruction. The interstitial deposition of collagen, α-SMA and TGF-β1 expression, and macrophage infiltration were dramatically decreased when P311 was knocked out. Moreover, TGFβ/Smad signaling had a critical effect on the promotion of renal fibrosis by P311. In conclusion, this study demonstrate that P311 plays a key role in renal fibrosis via TGFβ1/Smad signaling, which could be a novel target for the management of renal fibrosis.Entities:
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Year: 2015 PMID： 26616407 PMCID： PMC4663757 DOI： 10.1038/srep17032
Source DB: PubMed Journal: Sci Rep ISSN： 2045-2322 Impact factor: 4.379