Long-term treatment of swiss 3T3 fibroblasts with dexamethasone attenuates MAP kinase activation induced by insulin-like growth factor-I (IGF-I)

1996 ◽  
Vol 14 (2) ◽  
pp. 121-129
Author(s):  
Anders Hansson ◽  
Karin Hehenberger ◽  
Marja Thorén
Keyword(s):  
Growth Factor ◽  
Map Kinase ◽  
Term Treatment ◽  
Kinase Activation ◽  
Factor I ◽  
3T3 Fibroblasts ◽  
Long Term Treatment ◽  
Igf I ◽  
Swiss 3T3 Fibroblasts

Relative Deficiency in Circulating Levels of Insulin-Like Growth Factor I (IGF-I) During Long-Term Treatment with a GnRH Agonist

1997 ◽  
Vol 29 (09) ◽  
pp. 472-474
Author(s):  
C. Fiore ◽  
M. Dieli ◽  
S. Caschetto ◽  
A. Cirino ◽  
E. Cottini
Keyword(s):  
Growth Factor ◽  
Gnrh Agonist ◽  
Term Treatment ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Long Term Treatment ◽  
Igf I ◽  
Relative Deficiency ◽  
Circulating Levels

Insulin-like growth factor-I decreases serum lipoprotein(a) during long-term treatment of patients with Laron syndrome

Metabolism ◽  
1996 ◽  
Vol 45 (10) ◽  
pp. 1263-1266 ◽  
Author(s):  
Z. Laron ◽  
X.L. Wang ◽  
B. Klinger ◽  
A. Silbergeld ◽  
D.E.L. Wilcken
Keyword(s):  
Growth Factor ◽  
Term Treatment ◽  
Serum Lipoprotein ◽  
Insulin Like Growth Factor ◽  
Laron Syndrome ◽  
Lipoprotein A ◽  
Factor I ◽  
Long Term Treatment ◽  
Growth Factor I

scholarly journals Long-Term Treatment with Recombinant Insulin-Like Growth Factor (IGF)-I in Children with Severe IGF-I Deficiency due to Growth Hormone Insensitivity

2007 ◽  
Vol 92 (3) ◽  
pp. 902-910 ◽  
Author(s):  
Steven D. Chernausek ◽  
Philippe F. Backeljauw ◽  
James Frane ◽  
Joyce Kuntze ◽  
Louis E. Underwood ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Term Treatment ◽  
Insulin Like Growth Factor ◽  
Recombinant Insulin ◽  
Long Term Treatment ◽  
Igf I ◽  
Growth Hormone Insensitivity

scholarly journals Insulin Induces Heterologous Desensitization of G Protein-Coupled Receptor and Insulin-Like Growth Factor I Signaling by Downregulating β-Arrestin-1

2002 ◽  
Vol 22 (17) ◽  
pp. 6272-6285 ◽  
Author(s):  
Stéphane Dalle ◽  
Takeshi Imamura ◽  
David W. Rose ◽  
Dorothy Sears Worrall ◽  
Satoshi Ugi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Map Kinase ◽  
Insulin Treatment ◽  
Ectopic Expression ◽  
Wild Type ◽  
Factor I ◽  
Igf I ◽  
Heterologous Desensitization ◽  
Kinase Phosphorylation ◽  
G Protein Coupled

ABSTRACT β-Arrestin-1 mediates agonist-dependent desensitization and internalization of G protein-coupled receptors (GPCRs) and is also essential for GPCR mitogenic signaling. In addition, insulin-like growth factor I receptor (IGF-IR) endocytosis is facilitated by β-arrestin-1, and internalization is necessary for IGF-I-stimulated mitogen-activated protein (MAP) kinase activation. Here, we report that treatment of cells for 12 h with insulin (100 ng/ml) induces an ∼50% decrease in cellular β-arrestin-1 content due to ubiquitination of β-arrestin-1 and proteosome-mediated degradation. This insulin-induced decrease in β-arrestin-1 content was blocked by inhibition of phosphatidylinositol-3 kinase (PI-3 kinase) and MEK with wortmannin and PD98059, respectively. We also found a marked decrease in the association of β-arrestin-1 with the IGF-IR and a 55% inhibition of IGF-I-stimulated MAP kinase phosphorylation. In insulin-treated, β-arrestin-1-downregulated cells, there was complete inhibition of lysophosphatidic acid (LPA) or isoproterenol (ISO)-stimulated MAP kinase phosphorylation. This was associated with a decrease in β-arrestin-1 association with the β2-AR as well as a decrease in β-arrestin-1-Src and Src-β2-AR association. Ectopic expression of wild-type β-arrestin-1 in insulin-treated cells in which endogenous β-arrestin-1 had been downregulated rescued IGF-I- and LPA-stimulated MAP kinase phosphorylation. In conclusion, we found the following. (i) Chronic insulin treatment leads to enhanced β-arrestin-1 degradation. (ii) This downregulation of endogenous β-arrestin-1 is associated with decreased IGF-I-, LPA-, and ISO-mediated MAP kinase signaling, which can be rescued by ectopic expression of wild-type β-arrestin-1. (iii) Finally, these results describe a novel mechanism for heterologous desensitization, whereby insulin treatment can impair GPCR signaling, and highlight the importance of β-arrestin-1 as a target molecule for this desensitization mechanism.

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