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Involvement of the ERK/MAP kinase signalling pathway in milli-calpain activation and myogenic cell migration

Abstract : Recent research carried out in our laboratory has shown that IGF-1, TGF-beta1, and insulin were able to strongly stimulate myoblast migration by increasing milli-calpain expression and activity. However, the signalling pathways involved in these phenomena remain unknown. The aim of this study was to identify the signalling pathway(s) responsible for the effects of IGF-1, TGF-beta1, and insulin on myoblast migration and on milli-calpain expression and activity. For this purpose, wound healing assays were carried out in the presence of growth factors with or without specific inhibitors of ERK/MAP kinase and PI3K/Akt pathways. The results clearly showed that the inhibition of the ERK/MAP kinase pathway prevents the effects of growth factors on myoblast migration. Secondly, the expression and the activity of milli-calpain were studied in cells treated with growth factor, alone or with ERK/MAP kinase inhibitor. The results demonstrated that the up-regulation of milli-calpain expression and activity was mediated by the ERK/MAP kinase pathway. Finally, the possible implication of MyoD and myogenin, myogenic regulatory factors able to regulate milli-calpain expression, was studied. Taken together our results clearly showed that the ERK/MAP kinase signalling pathway is responsible for the effects of the three growth factors on myoblast migration and on milli-calpain expression and activity. On the opposite, the PI3K/Akt signalling pathway, MyoD and myogenin seem to be not implicated in these phenomena.
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https://hal-amu.archives-ouvertes.fr/hal-01740981
Contributor : Ludovic Leloup <>
Submitted on : Thursday, March 22, 2018 - 3:37:37 PM
Last modification on : Wednesday, October 14, 2020 - 3:50:30 AM

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Ludovic Leloup, Laetitia Daury, Germain Mazères, Patrick Cottin, Jean-Jacques Brustis. Involvement of the ERK/MAP kinase signalling pathway in milli-calpain activation and myogenic cell migration. International Journal of Biochemistry and Cell Biology, Elsevier, 2007, 39 (6), pp.1177 - 1189. ⟨10.1016/j.biocel.2007.03.003⟩. ⟨hal-01740981⟩

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