scholarly journals Acceleration of human myoblast fusion by depolarization: graded Ca2+ signals involved

Development ◽  
2003 ◽  
Vol 130 (15) ◽  
pp. 3437-3446 ◽  
Author(s):  
J.-H. Liu
Keyword(s):  
Myoblast Fusion ◽  
Human Myoblast

scholarly journals Human Myoblast Fusion Requires Expression of Functional Inward Rectifier Kir2.1 Channels

2001 ◽  
Vol 153 (4) ◽  
pp. 677-686 ◽  
Author(s):  
Jacqueline Fischer-Lougheed ◽  
Jian-Hui Liu ◽  
Estelle Espinos ◽  
David Mordasini ◽  
Charles R. Bader ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Muscle Development ◽  
Myoblast Fusion ◽  
Inward Rectifier ◽  
Resting Membrane Potential ◽  
Skeletal Muscle Development ◽  
K Channels ◽  
Window Current ◽  
Human Myoblast

Myoblast fusion is essential to skeletal muscle development and repair. We have demonstrated previously that human myoblasts hyperpolarize, before fusion, through the sequential expression of two K+ channels: an ether-à-go-go and an inward rectifier. This hyperpolarization is a prerequisite for fusion, as it sets the resting membrane potential in a range at which Ca2+ can enter myoblasts and thereby trigger fusion via a window current through α1H T channels.

scholarly journals Role of an inward rectifier K+current and of hyperpolarization in human myoblast fusion

1998 ◽  
Vol 510 (2) ◽  
pp. 467-476 ◽  
Author(s):  
J.-H. Liu ◽  
P. Bijlenga ◽  
J. Fischer-Lougheed ◽  
T. Occhiodoro ◽  
A. Kaelin ◽  
...  
Keyword(s):  
Myoblast Fusion ◽  
Inward Rectifier ◽  
K Current ◽  
Human Myoblast

scholarly journals Human myotube formation is determined by MyoD–Myomixer/Myomaker axis

2020 ◽  
Vol 6 (51) ◽  
pp. eabc4062
Author(s):  
Haifeng Zhang ◽  
Junfei Wen ◽  
Anne Bigot ◽  
Jiacheng Chen ◽  
Renjie Shang ◽  
...  
Keyword(s):  
Transcriptional Control ◽  
Myoblast Fusion ◽  
Low Grade ◽  
Fusion Model ◽  
Genetic Studies ◽  
Biochemical Assays ◽  
E Box ◽  
Human Muscles ◽  
Human Muscle Cells ◽  
Human Myoblast

Myoblast fusion is essential for formations of myofibers, the basic cellular and functional units of skeletal muscles. Recent genetic studies in mice identified two long-sought membrane proteins, Myomaker and Myomixer, which cooperatively drive myoblast fusion. It is unknown whether and how human muscles, with myofibers of tremendously larger size, use this mechanism to achieve multinucleations. Here, we report an interesting fusion model of human myoblasts where Myomaker is sufficient to induce low-grade fusion, while Myomixer boosts its efficiency to generate giant myotubes. By CRISPR mutagenesis and biochemical assays, we identified MyoD as the key molecular switch of fusion that is required and sufficient to initiate Myomixer and Myomaker expression. Mechanistically, we defined the E-box motifs on promoters of Myomixer and Myomaker by which MyoD induces their expression for multinucleations of human muscle cells. Together, our study uncovered the key molecular apparatus and the transcriptional control mechanism underlying human myoblast fusion.

scholarly journals Human Myoblast Differentiation: Ca2+ Channels are Activated by K+ Channels

Physiology ◽  
2002 ◽  
Vol 17 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Laurent Bernheim ◽  
Charles R. Bader
Keyword(s):  
Membrane Potential ◽  
Cellular Differentiation ◽  
Myoblast Fusion ◽  
Myoblast Differentiation ◽  
K Channels ◽  
Intracellular Ca ◽  
Human Myoblast ◽  
Ca2 Channels

In a paradigm of cellular differentiation, human myoblast fusion, we investigated how a Ca2+ influx, indispensable for fusion, is triggered. We show how newly expressed Kir2.1 K+ channels, via their hyperpolarizing effect on the membrane potential, generate a window Ca2+ current (mediated by a1H T-type Ca2+ channels), which causes intracellular Ca2+ to rise.

Human Myoblast Genome Therapies and Devices in Regenerative Medicine

2011 ◽  
Vol 1 (1) ◽  
pp. 88-117
Author(s):  
Peter K. Law ◽  
Danlin M. Law
Keyword(s):  
Regenerative Medicine ◽  
Human Myoblast

scholarly journals Specific blockers of myoblast fusion inhibit a soluble and not the membrane-associated metalloendoprotease in myoblasts.

1984 ◽  
Vol 259 (9) ◽  
pp. 5396-5399 ◽  
Author(s):  
C B Couch ◽  
W J Strittmatter
Keyword(s):  
Myoblast Fusion

scholarly journals TGFβ signalling acts as a molecular brake of myoblast fusion

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Julie Melendez ◽  
Daniel Sieiro ◽  
David Salgado ◽  
Valérie Morin ◽  
Marie-Julie Dejardin ◽  
...  
Keyword(s):  
Dynamic Control ◽  
Muscle Growth ◽  
Myoblast Fusion ◽  
In Vivo Studies ◽  
In Vitro Assays ◽  
Receptor Complex ◽  
Tgfβ Signalling ◽  
Molecular Brake

AbstractFusion of nascent myoblasts to pre-existing myofibres is critical for skeletal muscle growth and repair. The vast majority of molecules known to regulate myoblast fusion are necessary in this process. Here, we uncover, through high-throughput in vitro assays and in vivo studies in the chicken embryo, that TGFβ (SMAD2/3-dependent) signalling acts specifically and uniquely as a molecular brake on muscle fusion. While constitutive activation of the pathway arrests fusion, its inhibition leads to a striking over-fusion phenotype. This dynamic control of TGFβ signalling in the embryonic muscle relies on a receptor complementation mechanism, prompted by the merging of myoblasts with myofibres, each carrying one component of the heterodimer receptor complex. The competence of myofibres to fuse is likely restored through endocytic degradation of activated receptors. Altogether, this study shows that muscle fusion relies on TGFβ signalling to regulate its pace.

Human myoblast transfer: Immunological aspects

1991 ◽  
Vol 35 ◽  
pp. 65
Author(s):  
George Karpati ◽  
Montreal Myoblast Transfer Team
Keyword(s):  
Human Myoblast ◽  
Myoblast Transfer
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