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Transforming growth factor‐beta isoform expression in insulin‐like growth factor stimulated myogenesis
Author(s) -
Bosche William J.,
Ewton Daina Z.,
Florini James R.
Publication year - 1995
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041640213
Subject(s) - myogenesis , transforming growth factor beta , c2c12 , transforming growth factor, beta 3 , biology , transforming growth factor , growth factor , insulin like growth factor , insulin like growth factor receptor , beta (programming language) , downregulation and upregulation , tgf beta signaling pathway , myocyte , endocrinology , microbiology and biotechnology , gene isoform , medicine , cellular differentiation , insulin like growth factor 2 , morphogenesis , receptor , gene , tgf alpha , biochemistry , computer science , programming language
Transforming growth factor betas (TGF‐b̃s) are the defining members of a superfamily of small proteins that are involved in the regulation of development and morphogenesis in a wide array of systems. Previous studies have demonstrated that TGF‐b̃s both inhibit and, under specialized conditions, induce the differentiation of myoblasts. TGF‐b̃s have been shown to be secreted by mouse C2C12 myoblast cultures undergoing differentiation. Insulin‐like growth factors (IGFs) have also been shown to be secreted by myoblasts and to induce myogenesis. This study characterizes the effects of IGF treatment on the expression and secretion of TGF‐b̃s in the IGF‐sensitive L6A1 myoblast line. IGF downregulated the expression of TGF‐b̃3 in a concentration‐dependent manner at 24 and 48 hours; TGF‐b̃1 was not sensitive to IGF treatment at 24 hours but was downregulated by IGFs at 48 hours. This downregulation was mediated by the type I IGF receptor and modulated by IGF binding proteins secreted by the myoblasts. Some reexpression of TGF‐b̃1 and TGF‐b̃3 mRNAs was observed after extensive morphological differentiation had occurred. These results support the hypothesis that IGFs act through the IGF type I receptor as part of a concerted mechanism to modulate expression of the TGF‐b̃ genes, as part of a coordinated set of changes associated with terminal myogenic differentiation. © 1995 Wiley‐Liss, Inc.