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Cooperation of myocardin and smad2 in inducing differentiation of mesenchymal stem cells into smooth muscle cells
Author(s) -
Wang Nan,
Ren GuangDa,
Zhou Zhen,
Xu Yao,
Qin Tao,
Yu RuFa,
Zhang TongCun
Publication year - 2012
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1003
Subject(s) - myocardin , mesenchymal stem cell , smad , microbiology and biotechnology , biology , stem cell , cellular differentiation , in vivo , serum response factor , chemistry , transforming growth factor , gene , gene expression , genetics
Several reports demonstrated that mesenchymal stem cells (MSCs) might differentiate into smooth muscle cells (SMCs) in vitro and in vivo . It has been shown that myocardin protein is a strong inducer of smooth muscle genes and MSCs can differentiate into SMCs in response to transforming growth factor‐β (TGF‐β). However, the relationship or link between myocardin and TGF‐β3‐induced MSC differentiation has not been fully elucidated. Here, we demonstrated that both myocardin and TGF‐β3 were able to induce differentiation of rat bone marrow‐derived MSCs toward smooth‐muscle‐like cell types, as evidenced by increasing expression of SMC‐specific genes. Of note, myocardin cooperated with Smad2 to synergistically activate SM22α promoter and significantly enhance the expression of SM22α. Report assays with site‐direct mutation analysis of SM22α promoter demonstrated that myocardin and Smad2 coactivated SM22α promoter mainly depending on CArG box and less on smad binding elements (SBE) sites as well. These findings reveal the cooperation of myocardin and Smad2 in process of MSC differentiation into SMCs. © 2012 IUBMB Life, 64(4): 331–339, 2012