β2 Adrenergic receptor activation suppresses BMP-induced alkaline phosphatase expression in osteoblast-like MC3T3E1 cells.
β2 Adrenergic receptor activation suppresses BMP-induced alkaline phosphatase expression in osteoblast-like MC3T3E1 cells.
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β2 肾上腺素受体激活抑制成骨细胞样 MC3T3E1 细胞中 BMP 诱导的碱性磷酸酶表达。
DOI:
10.1002/jcb.25071
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发表时间:
2015
影响因子:
4
通讯作者:
M.
中科院分区:
文献类型:
--
作者:
Yamada;T.;Ezura;Y.;Hayata;T.;Moriya;S.;Shirakawa;J.;Notomi;T.;Arayal;S.;Kawasaki;M.;Izu;Y.;Harada;K.;and Noda;M.
β adrenergic stimulation suppresses bone formation in vivo while its actions in osteoblastic differentiation are still incompletely understood. We therefore examined the effects of β2adrenergic stimulation on osteoblast‐like MC3T3‐E1 cells focusing on BMP‐induced alkaline phosphatase expression. Morphologically, isoproterenol treatment suppresses BMP‐induced increase in the numbers of alkaline phosphatase‐positive small foci in the cultures of MC3T3‐E1 cells. Biochemically, isoproterenol treatment suppresses BMP‐induced enzymatic activity of alkaline phosphatase in a dose‐dependent manner. Isoproterenol suppression of alkaline phosphatase activity is observed even when the cells are treated with high concentrations of BMP. With respect to cell density, isoproterenol treatment tends to suppress BMP‐induced increase in alkaline phosphatase expression more in osteoblasts cultured at higher cell density. In terms of treatment protocol, continuous isoproterenol treatment is compared to cyclic treatment. Continuous isoproterenol treatment is more suppressive against BMP‐induced increase in alkaline phosphatase expression than cyclic regimen. At molecular level, isoproterenol treatment suppresses BMP‐induced enhancement of alkaline phosphatase mRNA expression. Regarding the mode of isoproterenol action, isoproterenol suppresses BMP‐induced BRE‐luciferase activity. These data indicate that isoproterenol regulates BMP‐induced alkaline phosphatase expression in osteoblast‐like MC3T3E1 cells. J. Cell. Biochem. 116: 1144–1152, 2015. © 2014 Wiley Periodicals, Inc.