Journal
SCIENTIFIC REPORTS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep32257
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Funding
- National Natural Science Foundation of China [81202162]
- Natural Science Foundation of Hebei Province [H201409115]
- Graduate Student Innovation Fund project in Hebei province [2015S03]
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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 alpha-tubulin (alpha-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-alpha 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 alpha-Ac-Tub in vivo and in vitro, which is related with deacetylase family member 6 (HDAC6) and alpha-tubulin acetyl transferase (alpha-TAT1). Our data suggest that alpha-Ac-Tub regulation by Ac-SDKP may potentially be a new anti-fibrosis mechanism.
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