scholarly journals Effects of Chromeceptin on Insulin-like Growth Factor II in Human Osteoblastic and Osteosarcoma Cells

2018 ◽  
Vol 4 (1) ◽  
pp. 59-67
Author(s):  
Rosemary Dziak ◽  
Dalia Nourah ◽  
That AlHousami ◽  
Dinh Nguyen

The insulin-like growth factor system is a complex regulatory system of insulin-like growth factors I and II (IGF-I and IGF-II) as well as their cell surface receptors and a family of insulin growth factor binding proteins (IGF-BPs). Despite extensive research on the IGF system in skeletal tissue, there is still not a complete understanding particularly of the role of IGF-II in the regulation of normal and pathological osseous cells in human skeletal biology. The purpose of this study was to further delineate the possible involvement of IGF-II in the regulation of human normal calvarial osteoblasts and G292 human osteosarcoma cellular activity using exogenously added IGF-II as well as a drug, Chromeceptin that has been shown in some other cellular systems to down regulate endogenous IGF-II levels.The results presented here show a similar dose dependent effect of Chromeceptin on inhibition of endogenous IGF-II levels (measured with an immunoassay) and cellular activity (measured with the MTT assay) in both the normal and osteosarcoma cells while small significant increases in activity with exogenously added IGF-II were observed only in the osteosarcoma cells. Moreover, IGF-BP1 levels (measured with an immunoassay) were shown to significantly increase in the G292 cells in a similar manner previously reported in other cell systems with only minor non-significant effects of exogenously added IGF-BP1 in the osteosarcoma cells studied here. These studies suggest that endogenous IGF-II is a critical regulator of activity in both normal and osteosarcoma cells and Chromeceptin can be an effective pharmacological agent for further studies on the role of the growth factor in human skeletal systems.

2020 ◽  
Vol 27 (42) ◽  
pp. 7256-7263
Author(s):  
Wenjing Ruan ◽  
Jing Deng ◽  
Kejing Ying

At least a proportion of patients suffering from chronic inflammatory airway diseases respond poorly to the bronchodilator and corticosteroid therapies. There is a need for the development of improved anti-inflammatory treatment. Insulin Growth Factor 1 (IGF1) and insulin participate in not only metabolism and glucose homeostasis, but also many other physiological and pathophysiological processes, including growth and inflammation. Recently, it was shown that not only the classical IGF1 and IGF1 Receptor (IGF1R), but also the other molecules in the IGF1/insulin network, including insulin, insulin-like growth factor-binding protein (IGFBP), and IGFBP protease, have roles in chronic inflammatory airway diseases. This review aims to provide a comprehensive insight into recent endeavors devoted to the role of the IGF1/insulin network in chronic inflammatory airway diseases. Its participation in airway inflammation, remodeling, and hyper-responsiveness (AHR), as well as acute exacerbation, has been conclusively demonstrated. Its possible relation to glucocorticoid insensitivity has also been indicated. A better understanding of the IGF1/insulin network by further bench-to-bedside research may provide us with rational clinical therapeutic approaches against chronic inflammatory airway diseases.


2009 ◽  
Vol 40 (4) ◽  
pp. 527-537 ◽  
Author(s):  
Ana Slipicevic ◽  
Geir Frode Øy ◽  
Inger Cecilie Askildt ◽  
Arild Holth ◽  
Ellen Hellesylt ◽  
...  

2013 ◽  
Vol 51 (08) ◽  
Author(s):  
E Kalideris ◽  
B Grüner ◽  
M Trajkovic-Arsic ◽  
P Mazur ◽  
RM Schmid ◽  
...  

1995 ◽  
Vol 766 (1 Receptor Acti) ◽  
pp. 402-408 ◽  
Author(s):  
D. LEROITH ◽  
H. WERNER ◽  
S. NEUENSCHWANDER ◽  
T. KALEBIC ◽  
L. J. HELMAN

Endocrinology ◽  
1994 ◽  
Vol 135 (5) ◽  
pp. 1845-1853 ◽  
Author(s):  
S Y Chun ◽  
H Billig ◽  
J L Tilly ◽  
I Furuta ◽  
A Tsafriri ◽  
...  

Endocrine ◽  
1997 ◽  
Vol 6 (1) ◽  
pp. 73-77 ◽  
Author(s):  
Serena H. Chen ◽  
Vanna Zanagnolo ◽  
Sangchai Preutthipan ◽  
Kenneth P. Roberts ◽  
Sandra B. Goodman ◽  
...  

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