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Role of Sulf1A in Wnt1- and Wnt6-induced growth regulation and myoblast hyper-elongation()

Sulf1A expression, which is a characteristic of embryonic muscle, is undetectable in mature muscle fibres and quiescent satellite cells, but is re-activated in vivo upon injury and in vitro following activation of satellite cells. Sulf1A is known to enhance canonical Wnt signalling, and its associat...

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Detalles Bibliográficos
Autores principales: Hitchins, L., Fletcher, F., Allen, S., Dhoot, G.K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3668513/
https://www.ncbi.nlm.nih.gov/pubmed/23772371
http://dx.doi.org/10.1016/j.fob.2012.11.007
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author Hitchins, L.
Fletcher, F.
Allen, S.
Dhoot, G.K.
author_facet Hitchins, L.
Fletcher, F.
Allen, S.
Dhoot, G.K.
author_sort Hitchins, L.
collection PubMed
description Sulf1A expression, which is a characteristic of embryonic muscle, is undetectable in mature muscle fibres and quiescent satellite cells, but is re-activated in vivo upon injury and in vitro following activation of satellite cells. Sulf1A is known to enhance canonical Wnt signalling, and its association with Wnt1-induced satellite cell proliferation in vitro in the present study further confirmed this. However, exogenous Wnt6 decreased satellite cell proliferation but promoted the adoption of a hyper-elongated cell morphology in myoblasts on isolated single fibres in culture. Such Wnt6-induced cellular hyper-elongation and inhibition of proliferation was found to be dependent upon Sulf1A, as treatment with Sulf1A neutralising antibodies abolished both these effects. This indicates that Sulf1A can regulate Wnt6 signalling and cellular differentiation in skeletal muscle.
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spelling pubmed-36685132013-06-14 Role of Sulf1A in Wnt1- and Wnt6-induced growth regulation and myoblast hyper-elongation() Hitchins, L. Fletcher, F. Allen, S. Dhoot, G.K. FEBS Open Bio Article Sulf1A expression, which is a characteristic of embryonic muscle, is undetectable in mature muscle fibres and quiescent satellite cells, but is re-activated in vivo upon injury and in vitro following activation of satellite cells. Sulf1A is known to enhance canonical Wnt signalling, and its association with Wnt1-induced satellite cell proliferation in vitro in the present study further confirmed this. However, exogenous Wnt6 decreased satellite cell proliferation but promoted the adoption of a hyper-elongated cell morphology in myoblasts on isolated single fibres in culture. Such Wnt6-induced cellular hyper-elongation and inhibition of proliferation was found to be dependent upon Sulf1A, as treatment with Sulf1A neutralising antibodies abolished both these effects. This indicates that Sulf1A can regulate Wnt6 signalling and cellular differentiation in skeletal muscle. Elsevier 2012-11-30 /pmc/articles/PMC3668513/ /pubmed/23772371 http://dx.doi.org/10.1016/j.fob.2012.11.007 Text en © 2013 The Authors http://creativecommons.org/licenses/BY-license/3.0/ This is an open-access article distributed under the terms of the Creative CommonsAttribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
spellingShingle Article
Hitchins, L.
Fletcher, F.
Allen, S.
Dhoot, G.K.
Role of Sulf1A in Wnt1- and Wnt6-induced growth regulation and myoblast hyper-elongation()
title Role of Sulf1A in Wnt1- and Wnt6-induced growth regulation and myoblast hyper-elongation()
title_full Role of Sulf1A in Wnt1- and Wnt6-induced growth regulation and myoblast hyper-elongation()
title_fullStr Role of Sulf1A in Wnt1- and Wnt6-induced growth regulation and myoblast hyper-elongation()
title_full_unstemmed Role of Sulf1A in Wnt1- and Wnt6-induced growth regulation and myoblast hyper-elongation()
title_short Role of Sulf1A in Wnt1- and Wnt6-induced growth regulation and myoblast hyper-elongation()
title_sort role of sulf1a in wnt1- and wnt6-induced growth regulation and myoblast hyper-elongation()
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3668513/
https://www.ncbi.nlm.nih.gov/pubmed/23772371
http://dx.doi.org/10.1016/j.fob.2012.11.007
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