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Title: Insulin-like growth factor-I-coupled mitogenic signaling in primary cultured human skeletal muscle cells and in C2C12 myoblasts. A central role of protein kinase Cdelta
Authors: Czifra, Gabriella ×
Tóth, Balázs István
Marincsák, Rita
Juhász, István
Kovács, Ilona
Acs, Péter
Kovács, László
Blumberg, Peter M
Bíró, Tamás #
Issue Date: Sep-2006
Publisher: Pergamon Press
Series Title: Cellular Signalling vol:18 issue:9 pages:1461-72
Abstract: In this study, we have investigated the effects of insulin-like growth factor-I (IGF-I) on cellular responses of primary human skeletal muscle cells and mouse C2C12 myoblasts. In human muscle, IGF-I stimulated proliferation and fusion of the cells and the expression of the differentiation marker desmin. These effects were completely inhibited by Rottlerin, the inhibitor of the protein kinase C (PKC)delta, but were not affected by the inhibition of the mitogen-activated protein kinase (MAPK) or the phosphatidylinositide 3-kinase (PI-3K) pathways. Furthermore, IGF-I initiated the selective translocation of PKCdelta to the nucleus. In C2C12 myoblasts, the growth-promoting effects of IGF-I were abrogated by inhibition of PKCdelta, but not by the inhibition of the PI-3K system. However, in contrast to the human data, the MAPK inhibitor PD098059 partially (yet significantly) also inhibited the action of IGF-I and, furthermore, IGF-I induced phosphorylation of the MAPK Erk-1/2. In addition, overexpression of constitutively active form of PKCdelta in C2C12 cells fully mimicked, whereas overexpression of kinase inactive mutant of the isoform prevented the action of IGF-I. Finally, the inhibition of PKCdelta suspended the IGF-I-induced phosphorylation of Erk-1/2 and, moreover, the inhibition of the MAPK pathway partially (yet significantly) inhibited the accelerated growth of C2C12 cells overexpressing PKCdelta. Taken together, these results demonstrate a novel, central and exclusive involvement of PKCdelta in mediating the action of IGF-I on human skeletal muscle cells, with an additional yet PKCdelta-dependent contribution of the MAPK pathway on C2C12 myoblasts.
URI: 
ISSN: 0898-6568
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Ion Channel Research
× corresponding author
# (joint) last author

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