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    MiR-124 Inhibits Myogenic Differentiation of Mesenchymal Stem Cells Via Targeting Dlx5 (2014)
    Wiley
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    Publication Date: 2014-04-16
    Description: MicroRNAs (miRNAs), including miR-1, miR-133, and miR-206, play a crucial role in muscle development by regulating muscle cell proliferation and differentiation. The aim of the present study was to define the effect of miR-124 on myogenic differentiation of mesenchymal stem cells (MSCs). The expression level of miR-124 in skeletal muscles was much lower than those in primary cultured bone marrow-derived MSCs and the bone, fat and brain tissues obtained from C57BL/6 mice. Myogenic stimuli significantly decreased the expression levels of miR-124 in mouse bone marrow-derived MSCs and C2C12 cells. Forced expression of miR-124 suppressed the expression of myogenic marker genes such as Myf5, Myod1, myogenin and myosin heavy chain and multinucleated myotube formation. Blockade of endogenous miR-124 with a hairpin inhibitor enhanced myogenic marker gene expression and myotube formation. During myogenic differentiation of MSCs and C2C12 cells, the levels of Dlx5, a known target of miR-124, were inversely regulated with those of miR-124. Furthermore, overexpression of Dlx5 increased myogenic differentiation, whereas knockdown of Dlx5 using siRNA inhibited myogenesis in C2C12 cells. These results suggest that miR-124 is a negative regulator of myogenic differentiation of MSCs and that upregulation of Dlx5 accompanied with downregulation of miR-124 by myogenic stimuli is necessary for the proper progression of myogenic differentiation. J. Cell. Biochem. © 2014 Wiley Periodicals, Inc.
    Electronic ISSN: 0091-7419
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Wiley
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  • 2
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    Tumor necrosis factor-α enhances the transcription of smad ubiquitination regulatory factor 1 in an activating protein-1- and Runx2-dependent manner (2012)
    Wiley
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    Publication Date: 2012-10-06
    Description: Smad Ubiquitination Regulatory Factor 1 (Smurf1) is an E3 ubiquitin ligase that negatively regulates osteoblast differentiation. Although tumor necrosis factor-α (TNF-α) has been shown to increase Smurf1 expression, the details of the regulatory mechanisms remain unclear. Here, we investigated the molecular mechanism by which TNF-α stimulates Smurf1 expression in C2C12 and primary cultured mouse calvarial cells. TNF-α treatment rapidly induced the activation of NF-κB and MAPKs. Smurf1 induction by TNF-α was blocked by the inhibition of JNK or ERK, while the inhibition of NF-κB and p38 MAPK had no effect on Smurf1 induction. TNF-α treatment or c-Jun overexpression enhanced the activity of a luciferase reporter that contained a 2.7 kb mouse Smurf1 promoter sequence. Site-directed mutagenesis of the Smurf1 reporter and chromatin immunoprecipitation analysis demonstrated that the activating protein-1 (AP-1) binding motif at -922 bp on the mouse Smurf1 promoter mediated TNF-α/JNK/AP-1-stimulated Smurf1 transcription. Interestingly, Smurf1 expression was not observed in Runx2-null mouse calvarial cells. When Runx2 was ectopically expressed in these cells, the basal and TNF-α-induced expression of Smurf1 was restored. Overexpression of Runx2 transactivated the Smurf1 promoter in a dose-dependent manner. Reporter and chromatin immunoprecipitation assays demonstrated that the Runx2-binding motif at -202 bp functioned in Runx2-mediated Smurf1 expression. ERK activation by TNF-α treatment or constitutively active MEK1 overexpression increased Smurf1 expression in a Runx2-dependent manner. These results suggest that the JNK/AP-1 and ERK/Runx2 signaling pathways mediate TNF-α-dependent Smurf1 transcription. J. Cell. Physiol. © 2012 Wiley Periodicals, Inc.
    Electronic ISSN: 1097-4652
    Topics: Biology , Medicine
    Published by Wiley
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