scholarly journals MicroRNA-29a in Adult Muscle Stem Cells Controls Skeletal Muscle Regeneration During Injury and Exercise Downstream of Fibroblast Growth Factor-2

Stem Cells ◽  
2016 ◽  
Vol 34 (3) ◽  
pp. 768-780 ◽  
Author(s):  
Artur Galimov ◽  
Troy L. Merry ◽  
Edlira Luca ◽  
Elisabeth J. Rushing ◽  
Amir Mizbani ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Muscle Stem Cells ◽  
Adult Muscle

The Role of Basic Fibroblast Growth Factor in Skeletal Muscle Regeneration

1992 ◽  
Vol 6 (1) ◽  
pp. 53-63 ◽  
Author(s):  
Mark Guthridge ◽  
Michael Wilson ◽  
Jane Cowling ◽  
Joseph Bertolini ◽  
Milton T. W. Hearn
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration ◽  
Fibroblast Growth

scholarly journals Gait disturbances and muscle dysfunction in fibroblast growth factor 2 knockout mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
C. Homer-Bouthiette ◽  
L. Xiao ◽  
Marja M. Hurley
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Muscle Strength ◽  
Fibroblast Growth Factor ◽  
Muscle Function ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Skeletal Muscle Function ◽  
Age Related ◽  
Gait Disturbances

AbstractFibroblast growth factor 2 (FGF2) is important in musculoskeletal homeostasis, therefore the impact of reduction or Fgf2 knockout on skeletal muscle function and phenotype was determined. Gait analysis as well as muscle strength testing in young and old WT and Fgf2KO demonstrated age-related gait disturbances and reduction in muscle strength that were exacerbated in the KO condition. Fgf2 mRNA and protein were significantly decreased in skeletal muscle of old WT compared with young WT. Muscle fiber cross-sectional area was significantly reduced with increased fibrosis and inflammatory infiltrates in old WT and Fgf2KO vs. young WT. Inflammatory cells were further significantly increased in old Fgf2KO compared with old WT. Lipid-related genes and intramuscular fat was increased in old WT and old Fgf2KO with a further increase in fibro-adipocytes in old Fgf2KO compared with old WT. Impaired FGF signaling including Increased β-Klotho, Fgf21 mRNA, FGF21 protein, phosphorylated FGF receptors 1 and 3, was observed in old WT and old Fgf2KO. MAPK/ ERK1/2 was significantly increased in young and old Fgf2KO. We conclude that Fgf2KO, age-related decreased FGF2 in WT mice, and increased FGF21 in the setting of impaired Fgf2 expression likely contribute to impaired skeletal muscle function and sarcopenia in mice.

Leukemia Inhibitory Factor and Fibroblast Growth Factor 2 Critically and Mutually Sustain Pluripotency of Rabbit Embryonic Stem Cells

2015 ◽  
Vol 24 (3) ◽  
pp. 319-338 ◽  
Author(s):  
Neng-Wen Lo ◽  
Payungsuk Intawicha ◽  
Yung-Tsung Chiu ◽  
Kun-Hsiung Lee ◽  
Hsi-Chi Lu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Leukemia Inhibitory Factor ◽  
Embryonic Stem ◽  
Inhibitory Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth

scholarly journals A Novel Mechanism of Sequestering Fibroblast Growth Factor 2 by Glypican in Lipid Rafts, Allowing Skeletal Muscle Differentiation

2010 ◽  
Vol 30 (7) ◽  
pp. 1634-1649 ◽  
Author(s):  
Jaime Gutiérrez ◽  
Enrique Brandan
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Lipid Rafts ◽  
Muscle Differentiation ◽  
Myoblast Fusion ◽  
Fibroblast Growth Factor 2 ◽  
Skeletal Muscle Differentiation ◽  
Fibroblast Growth ◽  
Raft Domains

ABSTRACT Heparan sulfate proteoglycans (HSPGs) are critical modulators of growth factor activities. Skeletal muscle differentiation is strongly inhibited by fibroblast growth factor 2 (FGF-2). We have shown that HSPGs present at the plasma membrane are expressed in myoblasts and are downregulated during muscle differentiation. An exception is glypican-1, which is present throughout the myogenic process. Myoblasts that do not express glypican-1 exhibit defective differentiation, with an increase in the receptor binding of FGF-2, concomitant with increased signaling. Glypican-1-deficient myoblasts show decreased expression of myogenin, the master gene that controls myogenesis, myosin, and the myoblast fusion index. Reversion of these defects was induced by expression of rat glypican-1. Glypican-1 is the only HSPG localized in lipid raft domains in myoblasts, resulting in the sequestration of FGF-2 away from FGF-2 receptors (FGFRs) located in nonraft domains. A chimeric glypican-1, containing syndecan-1 transmembrane and cytoplasmic domains, is located in nonraft domains interacting with FGFR-IV- and enhanced FGF-2-dependent signaling. Thus, glypican-1 acts as a positive regulator of muscle differentiation by sequestering FGF-2 in lipid rafts and preventing its binding and dependent signaling.

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