Amporn NuntapornsakKannikar WongdeeJirawan ThongbunchooNateetip KrishnamraNarattaphol CharoenphandhuMahidol UniversityBurapha University2018-09-242018-09-242010-01-01Cell Biochemistry and Function. Vol.28, No.1 (2010), 45-5110990844026364842-s2.0-74049109715https://repository.li.mahidol.ac.th/handle/20.500.14594/28810Activation of adrenergic receptors (AR) was demonstrated to result in either bone gain or bone loss depending on the activated AR subtypes and concentrations of agonists used. While β2-AR agonist was extensively investigated as an osteopenic agent, effects of β3-AR activation on osteoblasts were still elusive. Rat osteoblast-like UMR106 cells were herein found to express several AR subtypes, including β3-AR. After exposure to a low-dose β3-AR agonist BRL37344 (10 nmol L-1), UMR106 cells downregulated the mRNA expression of transcription factors Runx2 and Dlx5, which are important for initiation of osteoblast differentiation. Low-dose BRL37344 also decreased the expression ratio of receptor activator of nuclear factor kB ligand (RANKL) over osteoprotegerin (OPG), suggesting the protective effect of β3-AR agonist against bone resorption. Alkaline phosphatase expression was markedly decreased, whereas expressions of osteocalcin and osteopontin were increased by 100 nmol L-1 BRL37344, indicating that β3-AR activation could accelerate the transition of matrix maturation stage to mineralization stage. In conclusion, b3-AR activation in rat osteoblasts induced alteration in the expression of osteoblast-related transcription factor genes as well as genes required for bone formation and resorption. The present results also suggest that, besides β2-AR, β3-AR is another AR subtype responsible for the sympathetic nervous system-induced bone remodeling. Copyright © 2009 John Wiley & Sons, Ltd.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1002/cbf.1617