scholarly journals Magnesium deficiency up-regulates Myod expression in rat skeletal muscle and C2C12 myogenic cells

2011 ◽  
Vol 29 (7) ◽  
pp. 577-581 ◽  
Author(s):  
Yuuma Furutani ◽  
Masayuki Funaba ◽  
Tohru Matsui
Keyword(s):  
Skeletal Muscle ◽  
Magnesium Deficiency ◽  
Rat Skeletal Muscle ◽  
Myogenic Cells ◽  
C2c12 Myogenic Cells ◽  
Myod Expression

scholarly journals Functional skeletal muscle constructs from transdifferentiated human fibroblasts

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bin Xu ◽  
Allison Siehr ◽  
Wei Shen
Keyword(s):  
Skeletal Muscle ◽  
Disease Modeling ◽  
Myogenic Differentiation ◽  
Human Fibroblasts ◽  
Dermal Fibroblasts ◽  
Patient Specific ◽  
Myogenic Cells ◽  
Tissue Constructs ◽  
Contractile Forces ◽  
Myod Expression

AbstractTransdifferentiation of human non-muscle cells directly into myogenic cells by forced expression of MyoD represents one route to obtain highly desirable human myogenic cells. However, functional properties of the tissue constructs derived from these transdifferentiated cells have been rarely studied. Here, we report that three-dimensional (3D) tissue constructs engineered with iMyoD-hTERT-NHDFs, normal human dermal fibroblasts transduced with genes encoding human telomerase reverse transcriptase and doxycycline-inducible MyoD, generate detectable contractile forces in response to electrical stimuli upon MyoD expression. Withdrawal of doxycycline in the middle of 3D culture results in 3.05 and 2.28 times increases in twitch and tetanic forces, respectively, suggesting that temporally-controlled MyoD expression benefits functional myogenic differentiation of transdifferentiated myoblast-like cells. Treatment with CHIR99021, a Wnt activator, and DAPT, a Notch inhibitor, leads to further enhanced contractile forces. The ability of these abundant and potentially patient-specific and disease-specific cells to develop into functional skeletal muscle constructs makes them highly valuable for many applications, such as disease modeling.

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