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Examination of FGF2‐dependent proliferation in muscle precursor cells isolated from 3‐mo‐old and 32‐mo‐old rats: Implication for regrowth, repair, and regeneration of skeletal muscle
Author(s) -
Jump Seth S,
Childs Tom E,
Zwetsloot Kevin A,
Booth Frank W,
Lees Simon J
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.146
Subject(s) - skeletal muscle , mapk/erk pathway , regeneration (biology) , microbiology and biotechnology , fibroblast growth factor , medicine , endocrinology , cell growth , biology , chemistry , phosphorylation , receptor , biochemistry
Muscle precursor cells (MPCs) are located between the basal lamina and sarcolemma. MPCs are activated by stimuli such as exercise or muscle injury, and MPC proliferation is required for regrowth, repair, and regeneration of skeletal muscle. Fibroblast growth factor 2 (FGF2) is known to play a role in skeletal muscle repair and stimulates the proliferation of MPCs through the activation of the MAPK (MEK/ERK 1/2) pathway. Since aged skeletal muscle is characterized by impairments in regrowth, repair, and regeneration, it was hypothesized that MPCs isolated from 32‐mo‐old animals would have a blunted FGF2‐dependent proliferation compared to 3‐mo‐old animals. In response to multiple doses of FGF2 stimulation, MPCs from aged animals have lower cell number (0.1, 0.5, 1.0, 2.5, 5 ng/ml) and attenuated BrdU incorporation (1, 2.5, 5, 10, 100 ng/ml) compared to MPCs from young animals (p < .05). FGF receptor 1–4 mRNAs were not different in MPCs between 3‐mo‐old and 32‐mo‐old animals. Western blot data indicated no differences in phosphorylated and total MEK and phosphorylated and total ERK1/2 of MPCs between 3‐mo‐old and 32‐mo‐old animals. It is possible that there are age‐associated differences in downstream targets of ERK 1/2 or alternate FGF2‐dependent pathways which diminish proliferation of MPCs from old rats. Support: 5T32AR048523 and 5R01AG018780, National Institute of Health.