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Department of Cell and Molecular Biology, University of
Braunschweig, 38106 Braunschweig, Germany
Fibroblast growth factor-6 (FGF-6) belongs to a family of
cytokines that control cell proliferation, cell differentiation, and
morphogenetic events. Individual FGFs are either expressed widely or in
a restricted pattern during embryonic, fetal, and adult life. FGF-6
exhibits a restricted expression profile predominantly in the myogenic
lineage. Important functions in wound healing and tissue regeneration
have been proposed for various FGFs in the past, although data from
knockout mice have not supported this view. We have inactivated the
FGF-6 gene in mice to investigate the role of FGF-6 in skeletal muscle
development and regeneration. Wild-type mice up-regulate FGF-6 after
skeletal muscle injuries and completely restore experimentally damaged
skeletal muscle. In contrast, FGF-6(
/) mutant
mice show a severe regeneration defect with fibrosis and myotube
degeneration. The number of MyoD- and Myogenin-expressing activated
satellite cells after injury were significantly reduced in mutants.
This reduction was not caused by a reduced pool of quiescent satellite
cells but presumably by a lack of activation or proliferation.
Interbreeding of FGF-6(/) mutants with mdx mice
leads to striking dystrophic changes in skeletal muscles of double
homozygous mice characterized by myotube degeneration, the presence of
large amounts of mononuclear cells, and deposition of collagen. RNA
analysis revealed an up-regulation of MyoD mRNA in mdx but not in
FGF-6(/)/mdx double mutant mice. We
conclude that FGF-6 is a critical component of the muscle regeneration machinery in mammals, possibly by stimulating or activating satellite cells.
[Key Words: FGF-6; muscle regeneration; MyoD; mdx]
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