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First published online October 11, 2005
doi: 10.1242/10.1242/jcs.02602

Journal of Cell Science 118, 4813-4821 (2005)
Published by The Company of Biologists 2005
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Research Article

Evidence that satellite cell decrement contributes to preferential decline in nuclear number from large fibres during murine age-related muscle atrophy

Andrew S. Brack*, Heidi Bildsoe and Simon M. Hughes{ddagger}

MRC Centre for Developmental Neurobiology and Randall Division for Cell and Molecular Biophysics, New Hunt's House, King's College London, London, SE1 1UL, UK

{ddagger} Author for correspondence (e-mail: simon.hughes{at}kcl.ac.uk)

Accepted 14 August 2005

Skeletal muscle fibres are multinucleate syncitial cells that change size during adult life depending on functional demand. The relative contribution of change in nuclear number and/or cell growth to fibre size change is unclear. We report that nuclei/unit length decreases in larger fibres during skeletal muscle ageing. This leads to an increased size of nuclear domain (quantity of cytoplasm/number of nuclei within that cytoplasm). Initially, larger fibres have more satellite cells than small fibres, but this advantage is lost as satellite cells decline with age. These changes are accompanied by an overall decline in fibre size, returning domain size to the normal range. Exacerbated loss of fibre nuclei per unit length during ageing of myoD-null mice provides the first experimental support for the hypothesis that a satellite cell defect causes inadequate nuclear replacement. We propose a model in which a decline in satellite cell function and/or number during ageing leads to a loss of nuclei from large fibres and an associated domain size increase that triggers cytoplasmic atrophy through the normal cell-size-regulating machinery.

Key words: Muscle, Ageing, Fibre, Myoblast, Satellite cell, MyoD


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