Insulin-like growth factor (IGF)-II regulates CCAAT/enhancer binding protein α expression via phosphatidyl-inositol 3 kinase in human hepatoblastoma cell lines

2007 ◽  
Vol 102 (1) ◽  
pp. 161-170 ◽  
Author(s):  
Minoru Tomizawa ◽  
Hiromitsu Saisho
Keyword(s):  
Growth Factor ◽  
Cell Lines ◽  
Binding Protein ◽  
Phosphatidyl Inositol ◽  
Insulin Like Growth Factor ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

scholarly journals CCAAT/Enhancer-binding Protein δ Is a Critical Regulator of Insulin-like Growth Factor-I Gene Transcription in Osteoblasts

1999 ◽  
Vol 274 (15) ◽  
pp. 10609-10617 ◽  
Author(s):  
Yutaka Umayahara ◽  
Julia Billiard ◽  
Changhua Ji ◽  
Michael Centrella ◽  
Thomas L. McCarthy ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gene Transcription ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein ◽  
Growth Factor I ◽  
I Gene

scholarly journals CCAAT/Enhancer-binding Protein δ Activates Insulin-like Growth Factor-I Gene Transcription in Osteoblasts

1997 ◽  
Vol 272 (50) ◽  
pp. 31793-31800 ◽  
Author(s):  
Yutaka Umayahara ◽  
Changhua Ji ◽  
Michael Centrella ◽  
Peter Rotwein ◽  
Thomas L. McCarthy
Keyword(s):  
Growth Factor ◽  
Gene Transcription ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein ◽  
Growth Factor I ◽  
I Gene

scholarly journals Time- and Dose-Related Interactions between Glucocorticoid and Cyclic Adenosine 3′,5′-Monophosphate on CCAAT/Enhancer-Binding Protein-Dependent Insulin-Like Growth Factor I Expression by Osteoblasts1

Endocrinology ◽  
2000 ◽  
Vol 141 (1) ◽  
pp. 127-137 ◽  
Author(s):  
Thomas L. McCarthy ◽  
Changhua Ji ◽  
Yun Chen ◽  
Kenneth Kim ◽  
Michael Centrella
Keyword(s):  
Protein Synthesis ◽  
Growth Factor ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Enhancer Binding Protein ◽  
Igf I ◽  
Ccaat Enhancer Binding Protein ◽  
Growth Factor I ◽  
I Gene

Abstract Glucocorticoid has complex effects on osteoblasts. Several of these changes appear to be related to steroid concentration, duration of exposure, or specific effects on growth factor expression or activity within bone. One important bone growth factor, insulin-like growth factor I (IGF-I), is induced in osteoblasts by hormones such as PGE2 that increase intracellular cAMP levels. In this way, PGE2 activates transcription factor CCAAT/enhancer-binding protein-δ (C/EBPδ) and enhances its binding to a specific control element found in exon 1 in the IGF-I gene. Our current studies show that preexposure to glucocorticoid enhanced C/EBPδ and C/EBPβ expression by osteoblasts and thereby potentiated IGF-I gene promoter activation in response to PGE2. Importantly, this directly contrasts with inhibitory effects on IGF-I expression that result from sustained or pharmacologically high levels of glucocorticoid exposure. Consistent with the stimulatory effect of IGF-I on bone protein synthesis, pretreatment with glucocorticoid sensitized osteoblasts to PGE2, and in this context significantly enhanced new collagen and noncollagen protein synthesis. Therefore, pharmacological levels of glucocorticoid may reduce IGF-I expression by osteoblasts and cause osteopenic disease, whereas physiological transient increases in glucocorticoid may permit or amplify the effectiveness of hormones that regulate skeletal tissue integrity. These events appear to converge on the important role of C/EBPδ and C/EBPβ on IGF-I expression by osteoblasts.

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