Inhibition of mechanosensitive cation channels inhibits myogenic differentiation by suppressing the expression of myogenic regulatory factors and caspase‐3 activity

2005 ◽  
Vol 19 (14) ◽  
pp. 1986-1997 ◽  
Author(s):  
Nia Wedhas ◽  
Henry J. Klamut ◽  
Charu Dogra ◽  
Apurva K. Srivastava ◽  
Subburaman Mohan ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Myogenic Differentiation ◽  
Cation Channels ◽  
Myogenic Regulatory Factors ◽  
Regulatory Factors

Myogenic regulatory factors regulate M-cadherin expression by targeting its proximal promoter elements

2010 ◽  
Vol 428 (2) ◽  
pp. 223-233 ◽  
Author(s):  
Sheng Pin Hsiao ◽  
Shen Liang Chen
Keyword(s):  
Cell Adhesion ◽  
Transcription Initiation ◽  
Myogenic Differentiation ◽  
Initiation Site ◽  
Proximal Promoter ◽  
Myogenic Regulatory Factors ◽  
Regulatory Factors ◽  
Cell Cell

M- and N-cadherin are members of the Ca2+-dependent cell–cell adhesion molecule family. M-cadherin is expressed predominantly in developing skeletal muscles and has been implicated in terminal myogenic differentiation, particularly in myoblast fusion. N-cadherin-mediated cell–cell adhesion also plays an important role in skeletal myogenesis. In the present study, we found that both genes were differentially expressed in C2C12 and Sol8 myoblasts during myogenic differentiation and that the expression of M-cadherin was preferentially enhanced in slow-twitch muscle. Interestingly, most MRFs (myogenic regulatory factors) significantly activated the promoter of M-cadherin, but not that of N-cadherin. In line with this, overexpression of MyoD in C3H10T1/2 fibroblasts strongly induced endogenous M-cadherin expression. Promoter analysis in silico and in vitro identified an E-box (from −2 to +4) abutting the transcription initiation site within the M-cadherin promoter that is bound and differentially activated by different MRFs. The activation of the M-cadherin promoter by MRFs was also modulated by Bhlhe40 (basic helix–loop–helix family member e40). Finally, chromatin immunoprecipitation proved that MyoD as well as myogenin binds to the M-cadherin promoter in vivo. Taken together, these observations identify a molecular mechanism by which MRFs regulate M-cadherin expression directly to ensure the terminal differentiation of myoblasts.

scholarly journals The Homeodomain Protein Barx2 Promotes Myogenic Differentiation and Is Regulated by Myogenic Regulatory Factors

2002 ◽  
Vol 278 (10) ◽  
pp. 8269-8278 ◽  
Author(s):  
Robyn Meech ◽  
Helen Makarenkova ◽  
David B. Edelman ◽  
Frederick S. Jones
Keyword(s):  
Myogenic Differentiation ◽  
Homeodomain Protein ◽  
Myogenic Regulatory Factors ◽  
Regulatory Factors

scholarly journals More Than One-to-Four via 2R: Evidence of an Independent Amphioxus Expansion and Two-Gene Ancestral Vertebrate State for MyoD-Related Myogenic Regulatory Factors (MRFs)

2020 ◽  
Vol 37 (10) ◽  
pp. 2966-2982 ◽  
Author(s):  
Madeleine E Aase-Remedios ◽  
Clara Coll-Lladó ◽  
David E K Ferrier
Keyword(s):  
Gene Duplication ◽  
Myogenic Differentiation ◽  
Gene Families ◽  
Detailed Knowledge ◽  
Myogenic Regulatory Factors ◽  
Regulatory Factors ◽  
Ancestral Function ◽  
Gene Duplication And Loss ◽  
New Type ◽  
Bhlh Transcription Factors

Abstract The evolutionary transition from invertebrates to vertebrates involved extensive gene duplication, but understanding precisely how such duplications contributed to this transition requires more detailed knowledge of specific cases of genes and gene families. Myogenic differentiation (MyoD) has long been recognized as a master developmental control gene and member of the MyoD family of bHLH transcription factors (myogenic regulatory factors [MRFs]) that drive myogenesis across the bilaterians. Phylogenetic reconstructions within this gene family are complicated by multiple instances of gene duplication and loss in several lineages. Following two rounds of whole-genome duplication (2R WGD) at the origin of the vertebrates, the ancestral function of MRFs is thought to have become partitioned among the daughter genes, so that MyoD and Myf5 act early in myogenic determination, whereas Myog and Myf6 are expressed later, in differentiating myoblasts. Comparing chordate MRFs, we find an independent expansion of MRFs in the invertebrate chordate amphioxus, with evidence for a parallel instance of subfunctionalization relative to that of vertebrates. Conserved synteny between chordate MRF loci supports the 2R WGD events as a major force in shaping the evolution of vertebrate MRFs. We also resolve vertebrate MRF complements and organization, finding a new type of vertebrate MRF gene in the process, which allowed us to infer an ancestral two-gene state in the vertebrates corresponding to the early- and late-acting types of MRFs. This necessitates a revision of previous conclusions about the simple one-to-four origin of vertebrate MRFs.

Expression of myogenic regulatory factors (MRFs) in human neuromuscular disorders

1997 ◽  
Vol 23 (6) ◽  
pp. 475-482 ◽  
Author(s):  
M. Olive ◽  
J. A. Martinez-Matos ◽  
P. Pirretas ◽  
M. Povedano ◽  
C. Navarro ◽  
...  
Keyword(s):  
Neuromuscular Disorders ◽  
Myogenic Regulatory Factors ◽  
Regulatory Factors

TPA-Induced Differentiation of Human Rhabdomyosarcoma Cells: Expression of the Myogenic Regulatory Factors

1993 ◽  
Vol 208 (1) ◽  
pp. 209-217 ◽  
Author(s):  
M. Bouché ◽  
M.I. Senni ◽  
A.M. Grossi ◽  
F. Zappelli ◽  
M. Polimeni ◽  
...  
Keyword(s):  
Myogenic Regulatory Factors ◽  
Induced Differentiation ◽  
Regulatory Factors

scholarly journals Research Note: Increased myostatin expression and decreased expression of myogenic regulatory factors in embryonic ages in a quail line with muscle hypoplasia

2021 ◽  
Vol 100 (4) ◽  
pp. 100978
Author(s):  
Dong-Hwan Kim ◽  
Young Min Choi ◽  
Yeunsu Suh ◽  
Sangsu Shin ◽  
Joonbum Lee ◽  
...  
Keyword(s):  
Research Note ◽  
Myogenic Regulatory Factors ◽  
Regulatory Factors

scholarly journals Myogenic regulatory factors Myf5 and Myod function distinctly during craniofacial myogenesis of zebrafish

2006 ◽  
Vol 299 (2) ◽  
pp. 594-608 ◽  
Author(s):  
Cheng-Yung Lin ◽  
Rong-Feng Yung ◽  
Hung-Chieh Lee ◽  
Wei-Ta Chen ◽  
Yau-Hung Chen ◽  
...  
Keyword(s):  
Myogenic Regulatory Factors ◽  
Regulatory Factors

Abstract 123: Ischemia Mediates Myogenic Progenitor Cell Dysfunction

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Matthew Fincher ◽  
David Abraham ◽  
Daryll Baker ◽  
Janice Tsui
Keyword(s):  
Skeletal Muscle ◽  
Western Blot ◽  
Satellite Cells ◽  
Progenitor Cell ◽  
Caspase 3 ◽  
Myogenic Differentiation ◽  
Critical Limb Ischaemia ◽  
Limb Ischaemia ◽  
Muscle Biopsies ◽  
Myogenic Progenitor

Introduction Treatment options for critical limb ischaemia (CLI) are limited. Recent evidence has suggested that even with successful revascularisation, patients often show little functional improvement. This has been attributed to a musculopathy that occurs in CLI. Myogenic progenitor satellite cells (SCs) provide skeletal muscle with an intrinsic ability to regenerate. It has been shown that there is an increase in SCs in ischaemic muscle, however their function in ischaemia is poorly understood and we hypothesize that ischaemia has a detrimental effect on SC function. Methods Gastrocnemius muscle biopsies were taken from CLI patients and compared with non ischaemic control biopsies. The phenotypical changes and frequency of satellite cells were investigated using PAX 7 immunohistochemistry and western blot. C2C12 myoblasts were used in vitro, to investigate the effect of ischaemia on muscle progenitor cell function. Myoblasts were exposed to simulated ischaemia for 24, 48 and 72hrs. Proliferation rates were assessed using an MTT assay. Differentiation and apoptosis were assessed by MYOD and cleaved caspase 3 western blotting respectively. Results There is an increased expression of PAX 7 in CLI muscle biopsies, shown by both immunostaining and western blot analysis, suggesting an increased number of SCs in ischaemic human skeletal muscle (p<0.05). Myoblasts cultured in ischaemic conditions demonstrated decreased cell proliferation, reduced myogenic differentiation (decreased MYOD expression), and increased apoptosis (increased cleaved caspase 3 expression). Conclusion Despite an upregulation of SCs in ischaemic tissue, their function is suppressed in ischaemic conditions and this may be contributing to the poor functional recovery of patients post revascularisation. Enhancement of muscle regeneration in ischaemia may be a useful therapeutic adjunct in the treatment of CLI.

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