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2015 ; 5
(ä): 17032
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P311 promotes renal fibrosis via TGF?1/Smad signaling
#MMPMID26616407
Yao Z
; Yang S
; He W
; Li L
; Xu R
; Zhang X
; Li H
; Zhan R
; Sun W
; Tan J
; Zhou J
; Luo G
; Wu J
Sci Rep
2015[Nov]; 5
(ä): 17032
PMID26616407
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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 ?-smooth muscle actin (?-SMA) and transforming growth factor beta1 (TGF?1)
expression. Subsequently, these results were verified in a mouse experimental
renal fibrosis model induced by unilateral ureteral obstruction. The interstitial
deposition of collagen, ?-SMA and TGF-?1 expression, and macrophage infiltration
were dramatically decreased when P311 was knocked out. Moreover, TGF?/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 TGF?1/Smad signaling, which could be a novel target for the management of
renal fibrosis.
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