ArticlePloS one2012
S100B engages RAGE or bFGF/FGFR1 in myoblasts depending on its own concentration and myoblast density. Implications for muscle regeneration.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 59 citations in OpenAlex.
- Grass carp S100A10a/10b, two skin wound-induced genes, augment epithelial cell proliferation and migration in vitro.Fish physiology and biochemistry · 2026Article
- The role of AGEs in skeletal muscle atrophy and the beneficial effects of exercise.Frontiers in medicine · 2025Review
- Lipid Priming of Adipose Mesenchymal Stromal Cells with Docosahexaenoic Acid: Impact on Cell Differentiation, Senescence and the Secretome Neuroregulatory Profile.Tissue engineering and regenerative medicine · 2025Article
- How S100B crosses brain barriers and why it is considered a peripheral marker of brain injury.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Interaction of S100A6 Protein with the Four-Helical Cytokines.Biomolecules · 2023Article
- Article
- Characterization of the microRNA transcriptomes and proteomics of cochlear tissue-derived small extracellular vesicles from mice of different ages after birth.Cellular and molecular life sciences : CMLS · 2022Article
- Skin Autofluorescence, a Noninvasive Biomarker for Advanced Glycation End-products, Is Associated With Sarcopenia.The Journal of clinical endocrinology and metabolism · 2022Observational
- Advanced Glycation End-Products in Skeletal Muscle Aging.Bioengineering (Basel, Switzerland) · 2021Review
- Emerging role of S100B protein implication in Parkinson's disease pathogenesis.Cellular and molecular life sciences : CMLS · 2021Review
- Friend or Foe: S100 Proteins in Cancer.Cancers · 2020Review
- RAGE Signaling in Skeletal Biology.Current osteoporosis reports · 2019Review
- Blood-brain barrier permeability and physical exercise.Journal of neuroinflammation · 2019Review
- RAGE in the pathophysiology of skeletal muscle.Journal of cachexia, sarcopenia and muscle · 2018Review
- Cellular and molecular mechanisms of sarcopenia: the S100B perspective.Journal of cachexia, sarcopenia and muscle · 2018Review
- Levels of S100B protein drive the reparative process in acute muscle injury and muscular dystrophy.Scientific reports · 2017Article
- Fibroblast growth factor 21 is required for beneficial effects of exercise during chronic high-fat feeding.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- S100B protein in skeletal muscle regeneration: regulation of myoblast and macrophage functions.European journal of translational myology · 2016Article
- Possible local stem cells activation by microcurrent application in experimentally injured soleus muscle.International journal of stem cells · 2014Article
- Joining S100 proteins and migration: for better or for worse, in sickness and in health.Cellular and molecular life sciences : CMLS · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In high-density myoblast cultures S100B enhances basic fibroblast growth factor (bFGF) receptor 1 (FGFR1) signaling via binding to bFGF and blocks its canonical receptor, receptor for advanced glycation end-products (RAGE), thereby stimulating proliferation and inhibiting differentiation. Here we show that upon skeletal muscle injury S100B is released from myofibers with maximum release at day 1 post-injury in coincidence with satellite cell activation and the beginning of the myoblast proliferation phase, and declining release thereafter in coincidence with reduced myoblast proliferation and enhanced differentiation. By contrast, levels of released bFGF are remarkably low at day 1 post-injury, peak around day 5 and decline thereafter. We also show that in low-density myoblast cultures S100B binds RAGE, but not bFGF/FGFR1 thereby simultaneously stimulating proliferation via ERK1/2 and activating the myogenic program via p38 MAPK. Clearance of S100B after a 24-h treatment of low-density myoblasts results in enhanced myotube formation compared with controls as a result of increased cell numbers and activated myogenic program, whereas chronic treatment with S100B results in stimulation of proliferation and inhibition of differentiation due to a switch of the initial low-density culture to a high-density culture. However, at relatively high doses, S100B stimulates the mitogenic bFGF/FGFR1 signaling in low-density myoblasts, provided bFGF is present. We propose that S100B is a danger signal released from injured muscles that participates in skeletal muscle regeneration by activating the promyogenic RAGE or the mitogenic bFGF/FGFR1 depending on its own concentration, the absence or presence of bFGF, and myoblast density.
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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.