Transforming growth factor-beta and forskolin increase all classes of insulin-like growth factor-I transcripts in normal human osteoblast-like cells.
In this study, we examined regulation of insulin-like growth factor I (IGF-I) gene expression and transcript splicing in normal human osteoblast-like cells. Previous studies in rat osteoblastic cells have indicated that transforming growth factor-beta (TGF-beta) inhibits IGF-I expression, whereas inducers of intracellular cAMP stimulate IGF-I expression. However, in human osteoblast-like cells both TGF-beta and forskolin increased IGF-I mRNA levels in a time- and dose-dependent manner. All 4 classes of IGF-I transcript that can result from alternate leader exon usage and splicing of the human IGF-I gene were induced proportionally. Although human osteoblasts increase IGF-I mRNA in response to important skeletal regulatory factors, some responses may be species-specific.
Okazaki
R
R
Endocrine Research Unit, Mayo Clinic, Rochester, MN 55905.
Durham
S K
SK
Riggs
B L
BL
Conover
C A
CA
D001483:Base Sequence; D003994:Bucladesine / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000235:genetics*; D007700:Kinetics; D008969:Molecular Sequence Data; D010006:Osteoblasts / Q000378:metabolism*; D012326:RNA Splicing / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000494:pharmacology*
D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D005576:Colforsin; D003994:Bucladesine; D007334:Insulin-Like Growth Factor I; D000242:Cyclic AMP