Activation of TGR5 promotes osteoblastic cell differentiation and mineralization.
Authors of this article are:
Wang Q, Wang G, Wang B, Yang H.
A summary of the article is shown below:
Impairment of normal osteoblast differentiation has been associated with bone loss-related disorders, such as osteoporosis. Takeda G-protein coupled receptor 5 (TGR5) has been identified as an important modulator of bile acid and energy homeostasis. Little information regarding the effects of TGR5 on osteoblastic bone formation and matrix mineralization has been reported before. In the current study, we found that TGR5 was expressed in osteoblast-like cell line MC3T3-E1 cells. Osteogenic medium (OM) stimulation promoted the expression of TGR5 in a dose-dependent manner. Notably, treatment with the specific TGR5 agonist GPBARA increased ALP activity, matrix mineralization, and expressions of osteoblastic differentiation marker genes, such as ALP, OCN, and Osx, by promoting the expression of Runx-2. Silencing of TGR5 by transfection with TGR5 siRNA abolished these effects. Also, we found that the AMPK/eNOS pathway was involved in this process. Blockage of AMPK activation using its specific inhibitor compound C abolished the effect of GPBARA-induced increase in ALP activity, matrix mineralization, and expressions of osteoblastic differentiation marker genes. The obtained results provide a new insight into the physiological function of TGR5 in bone formation and suggest that TGR5 might be a novel therapeutic target for bone diseases.
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This article is a good source of information and a good way to become familiar with topics such as:
AMPK;MC3T3-E1 cells;Osteoblast differentiation;Takeda G-protein coupled receptor 5
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