ArticleAmerican journal of physiology. Cell physiology2015
Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- CXCL14 Enhances Myocyte Fusion and Activates the FAK-ERK5 Signaling Pathway in Skeletal Muscle Stem Cells and Myoblasts.International journal of stem cells · 2026Article
- Tissue Engineered 3D Constructs for Volumetric Muscle Loss.Annals of biomedical engineering · 2024Review
- Machine learning inference of continuous single-cell state transitions during myoblast differentiation and fusion.Molecular systems biology · 2024Article
- Review
- Per1/Per2-Igf2 axis-mediated circadian regulation of myogenic differentiation.The Journal of cell biology · 2021Article
- HSP70 drives myoblast fusion during C2C12 myogenic differentiation.Biology open · 2020Article
- P38α-MAPK Signaling Inhibition Attenuates Soleus Atrophy during Early Stages of Muscle Unloading.International journal of molecular sciences · 2020Article
- Keratin Hydrogel Enhances In Vivo Skeletal Muscle Function in a Rat Model of Volumetric Muscle Loss.Tissue engineering. Part A · 2017Article
- Regulation of cell-cell fusion by nanotopography.Scientific reports · 2016Article
- Apoptosis signal-regulating kinase 1 mediates the inhibitory effect of hepatocyte nuclear factor-4α on hepatocellular carcinoma.Oncotarget · 2016Article
- p38 MAPK Signaling in Osteoblast Differentiation.Frontiers in cell and developmental biology · 2016Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The p38 MAP kinases play critical roles in skeletal muscle biology, but the specific processes regulated by these kinases remain poorly defined. Here we find that activity of p38α/β is important not only in early phases of myoblast differentiation, but also in later stages of myocyte fusion and myofibrillogenesis. By treatment of C2 myoblasts with the promyogenic growth factor insulin-like growth factor (IGF)-I, the early block in differentiation imposed by the p38 chemical inhibitor SB202190 could be overcome. Yet, under these conditions, IGF-I could not prevent the later impairment of muscle cell fusion, as marked by the nearly complete absence of multinucleated myofibers. Removal of SB202190 from the medium of differentiating myoblasts reversed the fusion block, as multinucleated myofibers were detected several hours later and reached ∼90% of the culture within 30 h. Analysis by quantitative mass spectroscopy of proteins that changed in abundance following removal of the inhibitor revealed a cohort of upregulated muscle-enriched molecules that may be important for both myofibrillogenesis and fusion. We have thus developed a model system that allows separation of myoblast differentiation from muscle cell fusion and should be useful in identifying specific steps regulated by p38 MAP kinase-mediated signaling in myogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.