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Multipotency of skeletal muscle stem cells on their native substrate and the expression of Connexin 43 during adoption of adipogenic and osteogenic fate

Elashry, M., Heimann, M., Wenisch, S., Patel, K. and Arnhold, S. (2017) Multipotency of skeletal muscle stem cells on their native substrate and the expression of Connexin 43 during adoption of adipogenic and osteogenic fate. Acta Histochemica, 119 (8). pp. 786-794. ISSN 0065-1281

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To link to this item DOI: 10.1016/j.acthis.2017.10.002

Abstract/Summary

Skeletal muscle contains a resident stem cell population called Satellite cells (SC) which have a huge capacity to regenerate damaged tissue. Transplantation of a single fiber consisting of less than ten cells is able to generate tens of thousands of myonuclei within a matter of a few weeks (Collins et al., 2005). SC take their name from their peripheral position relative to the muscle fiber (Mauro, 1961). They are located under the basal lamina, in direct contact with the sarcolemma of muscle fibers. In undamaged muscle, they are relatively metabolically inactive as indicated by their low cytoplasmic content and they exist in a quiescent state. However, they express certain markers including Pax7 that aid their identification (Zammit et al., 2006). Upon muscle damage, SC become activated by inducing a number of genes including MyoD that encodes a member of the Myogenic Determination Factor family (MRF) of transcriptions factors (Zammit et al., 2006). Activation of SC permits cell division as well as migration. Initially, SC migrate under the basal lamina but then take up a supra-basal position by remodeling their overlying extra-cellular matrix (Otto et al., 2011). Activated SC can either revert to their quiescent state by down-regulating MyoD while maintaining Pax7 or can commit to myogenic differentiation by shutting off Pax7 expression and inducing the expression of

Item Type:Article
Refereed:Yes
Divisions:Faculty of Life Sciences > School of Biological Sciences > Biomedical Sciences
ID Code:73227
Publisher:Elsevier

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