Insulin as a Potent Stimulator of Akt, ERK and Inhibin-βE Signaling in Osteoblast-Like UMR-106 Cells.
10.4062/biomolther.2016.030
- Author:
Mahesh RAMALINGAM
1
;
Yong Dae KWON
;
Sung Jin KIM
Author Information
1. Departments of Pharmacology and Toxicology, Metabolic Diseases Research Laboratory, Kyung Hee University, Seoul 02447, Republic of Korea. kimsj@khu.ac.kr
- Publication Type:Original Article
- Keywords:
Akt;
ERK;
Inhibin-βE;
Insulin;
UMR-106
- MeSH:
Glucose;
Homeostasis;
Humans;
Insulin*;
Islets of Langerhans;
Learning;
Memory;
Osteoblasts;
Phosphorylation;
Phosphotransferases;
Proto-Oncogene Proteins c-akt
- From:Biomolecules & Therapeutics
2016;24(6):589-594
- CountryRepublic of Korea
- Language:English
-
Abstract:
Insulin is a peptide hormone of the endocrine pancreas and exerts a wide variety of physiological actions in insulin sensitive tissues, such as regulation of glucose homeostasis, cell growth, differentiation, learning and memory. However, the role of insulin in osteoblast cells remains to be fully characterized. In this study, we demonstrated that the insulin (100 nM) has the ability to stimulate the phosphorylation of protein kinase B (Akt/PKB) and extracellular signal-regulated kinase (ERK) and the levels of inhibin-βE in the osteoblast-like UMR-106 cells. This insulin-stimulated activities were abolished by the PI3K and MEK1 inhibitors LY294002 and PD98059, respectively. This is the first report proving that insulin is a potential candidate that enables the actions of inhibin-βE subunit of the TGF-β family. The current investigation provides a foundation for the realization of insulin as a potential stimulator in survival signaling pathways in osteoblast-like UMR-106 cells.
