The tumour suppressor gene p53 is recognised as a central regulator of the cell cycle and apoptosis. Post-natally, p53 mutations are associated with many cancers and mice lacking p53 are prone to spontaneous tumour formation. The present study examines skeletal muscle formation in post-natal mice lacking p53 using two different models of skeletal muscle regeneration. The level of endogenous myogenic cell proliferation in mature skeletal muscle was examined and the time course of muscle regeneration after whole muscle transplantation or crush injury were compared in p53(-/-) and control C57BI/6J adult mice, using desmin and proliferating cell nuclear antigen (PCNA) immunohistochemistry and histological analysis. The pattern of inflammation, myoblast proliferation and myotube formation in regenerating p53(-/-) skeletal muscles appears normal and similar to those in control C57BI/6J muscle. These data indicate that p53 is not required for the regulation of myoblast proliferation, differentiation and myotube formation in vivo during myogenesis of adult skeletal muscle.
|Number of pages||6|
|Journal||International Journal of Developmental Biology|
|Issue number||4 SPEC.|
|Publication status||Published - 01 Dec 2002|
White, J. D., Rachel, C., Vermeulen, R., Davies, M., & Grounds, M. D. (2002). The role of p53 in vivo during skeletal muscle post-natal development and regeneration: Studies in p53 knockout mice. International Journal of Developmental Biology, 46(4 SPEC.), 577-582.