ArticleGrowth factors (Chur, Switzerland)1997
Influence of PDGF-BB on proliferation and transition through the MyoD-myogenin-MEF2A expression program during myogenesis in mouse C2 myoblasts.
Article in Growth factors (Chur, Switzerland), 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 56 citations in OpenAlex.
- Reduced myogenic differentiation capacity of satellite cell-derived myoblasts in male ICR mice compared with male C57BL/6 and BALB/c mice.In vitro cellular & developmental biology. Animal · 2026Article
- Inhibition of myotube formation by platelet-derived growth factor subunit B in QM7 cells.Animal bioscience · 2025Article
- Neural cell integration into 3D bioprinted skeletal muscle constructs accelerates restoration of muscle function.Nature communications · 2020Article
- Intrinsic muscle clock is necessary for musculoskeletal health.The Journal of physiology · 2015Article
- Myogenic-specific ablation of Fgfr1 impairs FGF2-mediated proliferation of satellite cells at the myofiber niche but does not abolish the capacity for muscle regeneration.Frontiers in aging neuroscience · 2015Article
- ELAVL1 modulates transcriptome-wide miRNA binding in murine macrophages.Cell reports · 2014Article
- Meat Science and Muscle Biology Symposium: stem cell niche and postnatal muscle growth.Journal of animal science · 2012Review
- Skeletal muscle satellite cells: background and methods for isolation and analysis in a primary culture system.Methods in molecular biology (Clifton, N.J.) · 2012Article
- Regulation of DMD pathology by an ankyrin-encoded miRNA.Skeletal muscle · 2011Article
- The depletion of skeletal muscle satellite cells with age is concomitant with reduced capacity of single progenitors to produce reserve progeny.Developmental biology · 2010Article
- CC family chemokines directly regulate myoblast responses to skeletal muscle injury.The Journal of physiology · 2008Article
- FGFR4 and its novel splice form in myogenic cells: Interplay of glycosylation and tyrosine phosphorylation.Journal of cellular physiology · 2008Article
- Defining the transcriptional signature of skeletal muscle stem cells.Journal of animal science · 2008Review
- Reflections on lineage potential of skeletal muscle satellite cells: do they sometimes go MAD?Critical reviews in eukaryotic gene expression · 2007Review
- Entry of muscle satellite cells into the cell cycle requires sphingolipid signaling.The Journal of cell biology · 2006Article
- Satellite-cell pool size does matter: defining the myogenic potency of aging skeletal muscle.Developmental biology · 2006Article
- The transition from proliferation to differentiation is delayed in satellite cells from mice lacking MyoD.Developmental biology · 1999Article
- Proliferative Dynamics and the Role of FGF2 During Myogenesis of Rat Satellite Cells on Isolated Fibers.Basic and applied myology : BAMArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We have previously demonstrated that PDGF-BB enhances proliferation of C2 myoblasts. This has led us to examine whether the mitogenic influence of PDGF-BB in the C2 model correlates with modulation of specific steps associated with myogenic differentiation. C2 myoblasts transiting through these differentiation specific steps were monitored via immunocytochemistry. We show that the influence of PDGF on enhancing cell proliferation correlates with a delay in the emergence of cells positive for sarcomeric myosin. We further monitored the influence of PDGF-BB on differentiation steps preceding the emergence of myosin+ cells. We demonstrate that mononucleated C2 cells first express MyoD (MyoD+/myogenin- cells) and subsequently, myogenin. Cells negative for both MyoD and myogenin (the phenotype preceding the MyoD+ state) were present at all times in culture and comprised the majority, if not all, of the cells which responded mitogenically to PDGF. Additionally, the frequency of the MyoD+/myogenin+ cell phenotype was reduced in cultures receiving PDGF, suggesting that PDGF can modulate the transition of the cells into the myogenin+ state. We determined that many of the myogenin+ cells subsequently become MEF2A+ and this phenomenon is not influenced by PDGF-BB. FGF-2 also enhanced the proliferation of C2 myoblasts and suppressed the appearance of the myogenin+ cells, but did not influence the subsequent transition into the MEF2A+ state. The study raises the possibility that PDGF-BB and FGF-2 might delay the transition of the C2 cells into the MyoD+/myogenin+ state by depressing a paracrine signal that enhances differentiation.
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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.