Faculty Opinions recommendation of Mechano-transduction in osteoblastic cells involves strain-regulated estrogen receptor alpha-mediated control of insulin-like growth factor (IGF) I receptor sensitivity to Ambient IGF, leading to phosphatidylinositol 3-kinase/AKT-dependent Wnt/LRP5 receptor-independent activation of beta-catenin signaling.

2010 ◽  
Author(s):  
Chantal Chenu
Keyword(s):  
Estrogen Receptor ◽  
Growth Factor ◽  
Estrogen Receptor Alpha ◽  
Osteoblastic Cells ◽  
Beta Catenin ◽  
Insulin Like Growth Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Receptor Sensitivity ◽  
Receptor Alpha ◽  
Igf I

Estrogen receptor alpha (ERα) and insulin-like growth factor I receptor (IGF-IR) cross-talk in the gonadotropic αT3-1 cell line

2007 ◽  
Vol 212 (3) ◽  
pp. 583-590 ◽  
Author(s):  
Frank Eertmans ◽  
Willem Dhooge ◽  
Olivier De Wever ◽  
Marc Bracke ◽  
Frank Comhaire ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Growth Factor ◽  
Cell Line ◽  
Cross Talk ◽  
Estrogen Receptor Alpha ◽  
Insulin Like Growth Factor ◽  
Receptor Alpha ◽  
Factor I ◽  
Growth Factor I

scholarly journals Insulin-like growth factor I rapidly enhances acid efflux from osteoblastic cells

1999 ◽  
Vol 277 (3) ◽  
pp. E423-E432 ◽  
Author(s):  
Anu Santhanagopal ◽  
S. Jeffrey Dixon
Keyword(s):  
Growth Factor ◽  
Bone Resorption ◽  
Osteoblastic Cells ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Phosphatidylinositol 3

Insulin-like growth factor I (IGF-I) is thought to stimulate bone resorption indirectly through a primary effect on osteoblasts, which in turn activate osteoclasts by as-yet-unidentified mechanisms. Small decreases in extracellular pH (pHo) dramatically increase the resorptive activity of osteoclasts. Our purpose was to characterize the effect of IGF-I on acid production by osteoblastic cells. When confluent, UMR-106 osteoblast-like cells and rat calvarial cells acidified the compartment beneath them. Superfusion with IGF-I caused a further decrease in pHo. To investigate the mechanism, we monitored acid efflux from subconfluent cultures. IGF-I rapidly increased net efflux of H+ equivalents in a concentration-dependent manner. IGF-II (10 nM) evoked a smaller response than IGF-I (10 nM). The response to IGF-I was partially dependent on extracellular Na+, but not glucose, and exhibited little if any desensitization. Wortmannin, an inhibitor of phosphatidylinositol 3-kinase, abolished the response to IGF-I but not to parathyroid hormone. Thus IGF-I enhances acid efflux from osteoblastic cells, via a signaling pathway dependent on activation of phosphatidylinositol 3-kinase. In vivo, acidification of the compartment between the osteogenic cell layer and the bone matrix may affect diverse processes, including mineralization and osteoclastic bone resorption.

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