Effect of N-acetyl-seryl-aspartyl-lysyl-proline on differentiation from pulmonary fibroblast to myofibroblast mediated by Rho-associated coiled-coil forming protein kinase pathway

To investigate whether N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) can inhibit the differentiation of pulmonary fibroblasts into myofibroblasts by regulating Rho-associated coiled-coil forming protein kinase (ROCK) pathway mediated by transforming growth factor-β1 (TGF-β1). Primary culture of pu...

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Published inZhonghua laodong weisheng zhiyebing zazhi Vol. 31; no. 9; p. 654
Main Authors Yuan, Yuan, Yang, Fang, Xu, Hong, Yu, Wan-ying, Sun, Yue, Deng, Hai-jing, Ma, Wen-dong, Wei, Zhong-qiu, Wang, Rui-min
Format Journal Article
LanguageChinese
Published China 01.09.2013
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Summary:To investigate whether N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) can inhibit the differentiation of pulmonary fibroblasts into myofibroblasts by regulating Rho-associated coiled-coil forming protein kinase (ROCK) pathway mediated by transforming growth factor-β1 (TGF-β1). Primary culture of pulmonary fibroblasts was performed by trypsinization method. Four generations of pulmonary fibroblasts were divided into control group, TGF-β-induced differentiation group, Y-27632 treatment group, and Ac-SDKP treatment group. The intracellular distributions of ROCK, serum response factor (SRF), and α-smooth muscle actin (α-SMA) were observed by confocal laser scanning microscopy. The protein expression of ROCK, SFR, α-SMA, and type I and type III collagen in pulmonary fibroblasts was measured by Western blot. The mRNA expression of ROCK, SFR, and α-SMA was measured by real-time quantitative PCR. Compared with the control group, the pulmonary fibroblasts stimulated by TGF-β1 had a lot of α-SMA antibody-labeled myofi
ISSN:1001-9391