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Publication : Gait disturbances and muscle dysfunction in fibroblast growth factor 2 knockout mice.

First Author  Homer-Bouthiette C Year  2021
Journal  Sci Rep Volume  11
Issue  1 Pages  11005
PubMed ID  34040128 Mgi Jnum  J:306282
Mgi Id  MGI:6713178 Doi  10.1038/s41598-021-90565-0
Citation  Homer-Bouthiette C, et al. (2021) Gait disturbances and muscle dysfunction in fibroblast growth factor 2 knockout mice. Sci Rep 11(1):11005
abstractText  Fibroblast 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 beta-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.
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