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Osteopontin-induced brown adipogenesis from white preadipocytes through a PI3K-AKT dependent signaling
Recent studies have shown that OPN (osteopontin) plays critical roles in cell survival, differentiation, bio-mineralization, cancer and cardiovascular remodeling. However, its roles in the differentiation of brown adipocytes and the underlying mechanisms remain unclear. Therefore, the aim of this st...
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Published in: | Biochemical and biophysical research communications 2015-04, Vol.459 (3), p.553-559 |
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Main Authors: | , , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Recent studies have shown that OPN (osteopontin) plays critical roles in cell survival, differentiation, bio-mineralization, cancer and cardiovascular remodeling. However, its roles in the differentiation of brown adipocytes and the underlying mechanisms remain unclear. Therefore, the aim of this study was to investigate the roles of OPN in the brown adipogenesis and the underlying mechanisms. It was shown that the OPN successfully induced the differentiation of 3T3-L1 white preadipocytes into the PRDM16+ (PRD1-BF1-RIZ1 homologous domain containing 16) and UCP-1+ (uncoupling protein-1) brown adipocytes in a concentration and time-dependent manner. Also, activation of PI3K (phosphatidylinositol 3-kinase)-AKT pathway was required for the OPN-induced brown adipogenesis. The findings suggest OPN plays an important role in promoting the differentiation of the brown adipocytes and might provide a potential novel therapeutic approach for the treatment of obesity and related disorders.
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•Osteopontin induces brown adipogenesis in a concentration and time-dependent manner.•Phosphorylation of AKT is required for osteopontin-induced brown adipogenesis.•Osteopontin-induced brown adipogenesis is via a PI3K-AKT dependent pathway.•These findings provide a potential therapeutic approach for obesity-related disorders. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2015.02.153 |