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Regulation of Mouse Embryonic Stem Cell Differentiation by p38α MAP Kinase
Author(s) -
Ye Jianming,
Ragan Suja,
Huang Faging,
Guo Yanlin
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a379
Subject(s) - microbiology and biotechnology , embryonic stem cell , cellular differentiation , biology , cell type , p38 mitogen activated protein kinases , stem cell , p19 cell , cell , stem cell marker , somatic cell , mitogen activated protein kinase , protein kinase a , kinase , adult stem cell , genetics , gene
p38 mitogen‐activated protein (MAP) kinase a (p38α) is a broadly expressed signaling molecule that regulates various cellular processes. Most studies of p38α have been focusing on adult somatic cells, but little is known about its function in stem cells. The objective of this study was to determine the role of p38α in mouse ES cell differentiation using protocols that allow ES cells to differentiate into different types of cells. We report here that p38α deficient (p38α+/− and p38α−/ −) were able to different into endothelial cells, smooth muscle cells (SMC), and neurons as judged by the expression of specific markers and expected morphology of these cell types. However, the relative levels of some markers expressed in cells differentiated from mutant ES cells were different from cells differentiated from wild‐type ES cells. The major finding of this study is that the expression of SMC markers, α‐actin (SMA) and SM22α, in cells derived from p38α−/ − ES cells was significantly increased. However, these cells displayed disorganized SMA filament structure as compared with the SMC differentiated from wild‐type ES cells. Our results suggested that p38α negatively regulates SMC marker expression and controls the organization of SMA. This is different from adult SMC differentiation where in most cases the activation of p38α is required for the expression of SMC markers, indicating that p38α may play different roles in adult SMC and embryonic SMC differentiation [Supported by NIH R21HL08273].