详细信息

β-mercaptoethanol promotes osteogenesis of human mesenchymal stem cells via sirt1-ERK pathway  ( SCI-EXPANDED收录 EI收录)  

文献类型:期刊文献

英文题名:β-mercaptoethanol promotes osteogenesis of human mesenchymal stem cells via sirt1-ERK pathway

作者:Liu, Jiaxing[1];Wang, Hui[1];Ren, Wenxia[1];Zhou, Yan[1];Ye, Zhaoyang[1];Tan, Wen-Song[1]

机构:[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, 130 Mei Long Rd,POB 309, Shanghai 200237, Peoples R China

年份:2020

卷号:72

期号:5

起止页码:695

外文期刊名:CYTOTECHNOLOGY

收录:;EI(收录号:20242616308145);WOS:【SCI-EXPANDED(收录号:WOS:000550634100001)】;

基金:This research was supported by the National Key Research and Development Program of China (Grant No. 2018YFC1105800), the National Natural Science Foundation of China (Grant No. 81671841), the Fundamental Research Funds for the Central Universities (Grant No. 22221818014).

语种:英文

外文关键词:Umbilical cord-derived mesenchymal stem cells; Osteogenic differentiation; beta-mercaptoethanol; sirt1; ERK

摘要:Human umbilical cord-derived mesenchymal stem cells (hUMSCs) hold strong self-renewal capacity and low immunogenicity, which have attracted attention as potential candidates for bone repair and regeneration. However, insufficient osteogenic differentiation markedly hinders the clinical applications of hUMSCs. In the present study, the effect of beta-mercaptoethanol (BME), a small molecule antioxidant which has been identified to regulate cell proliferation and differentiation, on osteogenic differentiation of hUMSCs and underlying signaling mechanism were investigated. The results indicated that under osteogenic induction conditions, BME treatment increased the alkaline phosphatase (ALP) activity and promoted calcium mineralization in hUMSCs. The gene and protein expression of osteogenesis-related markers such as ALP, osteopontin (OPN), osteocalcin (OCN) and collagen type I (COLI) were also significantly up-regulated. Besides, BME promoted the protein expression of silent information regulator type 1 (sirt1) and stimulated the activation of extracellular signal-related kinase (ERK), contributing to increased Runx2 expression. Furthermore, blocking the expression of sirt1 attenuated BME-enhanced ERK phosphorylation and osteogenic differentiation of hUMSCs. These results indicated that BME accelerated osteogenic differentiation of hUMSCs by activating the sirt1-ERK signaling pathway, thereby providing insights into the development of MSCs-based bone regeneration strategies.

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