IGF-1 enhances a store-operated Ca2+ channel in skeletal muscle myoblasts: involvement of a CD20-like protein.
Overexpression of IGF-1 in C2C12 myoblasts causes hypertrophy when myoblasts fuse to form myotubes, a response that requires elevated intracellular calcium. We show that myoblasts contain a store-operated Ca2+ channel (SOCC) whose activity is enhanced with IGF-1 overexpression. A membrane protein, CD20, can cause Ca2+ entry, which is increased by IGF-1. We therefore tested whether CD20 mediates the SOCC activity in myoblasts. An antibody to the extracellular loop of CD20 detected a protein in myoblasts and this antibody also inhibited Ca2+ entry through SOCC. Overexpression of CD20 in myoblasts increased SOCC activity. However, we could not detect mRNA for CD20 in myoblasts and an antibody to the intracellular C-terminus of CD20 was unable to detect CD20 in these cells. These studies demonstrate that CD20 is a novel SOCC or modulates SOCC activity. However, the SOCC activity observed in C2C12 myoblasts is mediated not by CD20, but by a CD20-like protein. Activation of this SOCC may contribute to IGF-1-induced hypertrophy in these cells.
Ju
Yue-Kun
YK
Department of Physiology, University of Sydney, NSW, Australia.
Wu
Ming-Jie
MJ
Chaulet
Herve
H
Marciniec
Tadeusz
T
Graham
Robert M
RM
Allen
David G
DG
D000818:Animals; D018951:Antigens, CD20 / Q000378:metabolism*; D015152:Blotting, Northern; D015153:Blotting, Western; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism*; D002478:Cells, Cultured; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D051379:Mice; D018482:Muscle, Skeletal / Q000166:cytology / Q000378:metabolism*; D032446:Myoblasts / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction
D018951:Antigens, CD20; D015220:Calcium Channels; D012333:RNA, Messenger; D007334:Insulin-Like Growth Factor I; D002118:Calcium