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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Sci+Rep
2016 ; 6
(ä): 32257
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Acetylated ?-Tubulin Regulated by N-Acetyl-Seryl-Aspartyl-Lysyl-Proline(Ac-SDKP)
Exerts the Anti-fibrotic Effect in Rat Lung Fibrosis Induced by Silica
#MMPMID27577858
Xiaojun W
; Yan L
; Hong X
; Xianghong Z
; Shifeng L
; Dingjie X
; Xuemin G
; Lijuan Z
; Bonan Z
; Zhongqiu W
; Ruimin W
; Brann D
; Fang Y
Sci Rep
2016[Aug]; 6
(ä): 32257
PMID27577858
show ga
Silicosis is the most serious occupational disease in China. The objective of
this study was to screen various proteins related to mechanisms of the
pathogenesis of silicosis underlying the anti-fibrotic effect of
N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) using proteomic profile analysis.
We also aimed to explore a potential mechanism of acetylated ?-tubulin (?-Ac-Tub)
regulation by Ac-SDKP. Two-dimensional electrophoresis (2-DE) and matrix-assisted
laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF/TOF MS)
were used to assess the different protein expression profiles between control and
silicosis rats treated with or without Ac-SDKP. Twenty-nine proteins were
identified to be potentially involved in the progression of silicosis and the
anti-fibrotic effect of Ac-SDKP. Our current study finds that 1) the lost
expression of Ac-Tub-? may be a new mechanism in rat silicosis; 2) treatment of
silicotic rats with N-acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits
myofibroblast differentiation and collagen deposition accompanied by stabilizing
the expression of ?-Ac-Tub in vivo and in vitro, which is related with
deacetylase family member 6 (HDAC6) and ?-tubulin acetyl transferase (?-TAT1).
Our data suggest that ?-Ac-Tub regulation by Ac-SDKP may potentially be a new
anti-fibrosis mechanism.