The effect of N-acetyl-seryl-aspartly-lysyl-proline on myofibroblast different iation
- VernacularTitle:N-乙酰基-丝氨酰-天门冬氨酰-赖氨酰-脯氨酸对肌成纤维细胞分化的作用
- Author:
Xinxin XUE
;
Shipu DU
;
Shifeng LI
;
Xiaojun WANG
;
Yan LIU
;
Haijing DENG
;
Dingjie XU
;
Hong XU
;
Fang YANG
- Publication Type:Journal Article
- Keywords:
N-acetyl-seryl-aspartyl-lysyl-proline;
Angiotensin Ⅱ;
Fibroblast;
Signal transduction pathway;
Collagen Ⅰ
- From:
Journal of Medical Postgraduates
2015;(2):131-135
- CountryChina
- Language:Chinese
-
Abstract:
[Abstract ] Objective Silicosis is one of the most serious occupational diseases in China .In this study,we explored the reg -ulatory effect of N-acetyl-seryl-aspartyl-lysyl-proline ( Ac-SDKP ) on angiotensin ( Ang ) Ⅱ-induced extracellular signal-regulated ki-nase ( ERK1/2) and Jun N-terminal kinase ( JNK) signals and its inhibitory effect on the differentiation of human embryonic lung MRC-5 fibroblasts to myofibroblasts via Ang Ⅱ-induced ERK1/2 and JNK signals . Methods Human embryonic lung MRC-5 fibro-blasts were induced by Ang Ⅱand pre-treated with the JNK signal inhibitor ( SP600125 ) , the ERK1/2 signal inhibitor ( PD98059 ) or Ac-SDKP.The proliferation of the cells was measured by MTT assay .The expressions of αS-MA, SRF, p-ERK1/2 and p-JNK were determined by immunocytochemical staining , and the expression levels of these proteins and collagen Ⅰwere detected by Western blot .Results The A value of Ang Ⅱ group (0.56 ±0.08) measured by MMT assay was 2.07 fold as control group ( 0.27 ±0.05 ). Pretreatment with SP600125 , PD98059 and Ac-SDKP, the A value were (0.39 ±0.02), (0.40 ±0.03) and (0.36 ±0 0.5) that had a statistical significance with Ang Ⅱgroup.The up-regulation of colla-gen type Ⅰ,α-SMA, SRF were induced by Ang Ⅱ by 4.50, 3.50 and 3.00 fold compared with control group.Moreover, the expression of p-ERK1/2 and p-JNK were increased as 6.71 and 7.90 fold as control. Pre-treatment with Ac-SDKP could inhibit p-JNK and p-ERK1/2 to 29.79% and 46.84% compared with AngⅡ group. Conclusion Ac -SDKP can inhibit the differentiation of human embryonic lung MRC-5 fibroblasts to myofibroblasts by regulating AngⅡ-induced JNK and ERK1/2 signals.
