Myocyte Enhancer Factor 2C (
MEF2C), playing a significant role during muscle growth [25], can express circRNA468 as shown in our study.
ZIP14-mediated zinc uptake in muscle progenitor cells represses the expression of MyoD and
Mef2c and blocks muscle-cell differentiation.
Cells subjected to cyclic strain expressed GATA-4, [beta]-MHC, NKx2.5, and
MEF2c. Gene expression was greatest in cells subjected to 10% strain.
The deletion of
Mef2C (at e9.5) alters embryonic vascular development thereby inducing vascular anomalies, with CHF1/Hey2 null mice (at e13.5) displaying minor anatomical changes in critical systemic arteries and disordered microvasculature.
Direct reprogramming of fibroblasts into cardiomyocyte-like cells was first reported in 2010 using viral overexpression of three important cardiac developmental transcription factors (TFs), Gata4,
Mef2c, and Tbx5 (GMT) in mouse cardiac and tail-tip fibroblasts [11].
MDSC: Myeloid-derived suppressor cell M-MDSC: Monocytic MDSC G-MDSC: Granulocytic MDSC DC: Dendritic cell HR1: Histamine receptor 1 BCL-XL: B-cell lymphoma XL TLR: Toll-like receptor ADAM: A disintegrin and metalloproteinase miRNA: MicroRNAs ROS: Reactive oxygen species
MEF2C: Myeloid enhancement factor 2C Arg-1: Arginase-1 Treg: Regulatory T cell SCLC: Small cell lung cancer NSCLC: Nonsmall cell lung cancer SWCNT: Single-walled carbon nanotubes ATRA: All-trans-retinoic acid SCF: Stem cell factor VEGF: Vascular endothelial growth factor COX2: Cyclooxygenase 2 EMT: Epithelial mesenchymal transition.
Rosengart, a team of researchers showed that administration of a cocktail made of transcription factors Gata4,
Mef2c and Tbx5 (GMT) resulted in less scar tissue, or fibrosis, and up to a 50 percent increase in cardiac function in small animal models of the disease.
Maiti et al., "
MEF2C ablation in endothelial cells reduces retinal vessel loss and suppresses pathologic retinal neovascularization in oxygen-induced retinopathy," The American Journal of Pathology, vol.
In this sense, genes like
MEF2C, mTOR, MYB, FOXM1, GATA3, FOXP3, BCL6, MNDA, POU2AF1,
MEF2C, or SMAD3 have been reported to potentially regulate more than one thousand genes, which are transcriptional master regulators (TMRs) [2,3].
Taylor et al., "Disruption of
MEF2C signaling and loss of sarcomeric and mitochondrial integrity in cancer-induced skeletal muscle wasting," Aging, vol.
The antibodies used in this study include FGF21 (1: 1000, Abcam, USA), MyoD (1: 500, Santa Cruz, USA), MyoG (1: 500, Santa Cruz, USA),
MEF2c (1: 500, Santa Cruz, USA), MHC (1: 500, Santa Cruz, USA), CDK4 (1:1000, CST, USA), P21 (1:1000, R&D, USA), P53 (CST) Cyclin D1 (1: 1000, R&D, USA), Cyclin D3 (1: 1000, R&D, USA), and tubulin (1: 1000, Abcam, USA), which were diluted with 5% BSA.
Inhibition of the NO pathway reduces the number of beating cell colonies as well as transcripts of Nkx2.5,
MEF2c, and genes of contractile proteins.
