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• W1561724648 abstract "Recent studies reported that serotonin (5-hydroxytryptamine, 5-HT) may be an endogenous paracrine and/or autocrine factor that is used for intercellular communication in bone cells and between multiple organs regulating bone homeostasis. In the present study, we showed that the administration of MDL11939, a selective 5-HT2A receptor antagonist, reduced bone mass in mice. The loss of bone mass in MDL11939-treated mice was associated with impaired bone formation in vivo, as demonstrated by the lower expression of osterix (Osx) and osteocalcin than that in vehicle-treated mice. On the other hand, no significant differences were observed in osteoclast numbers between MDL11939- and vehicle-treated mice. The pharmacological blockade of 5-HT2A receptor signaling significantly decreased alkaline phosphatase activity in osteoblastic cells. In addition, the knockdown of the 5-HT2A receptor by a siRNA treatment decreased Osx, but not Runx2 gene expression in MC3T3-E1 cells. These results suggest that 5-HT2A receptor signaling mediated bone mass by regulating osteoblast differentiation." @default.
• W1561724648 created "2016-06-24" @default.
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• W1561724648 date "2015-09-01" @default.
• W1561724648 modified "2023-10-14" @default.
• W1561724648 title "Modulation of osteoblast differentiation and bone mass by 5-HT2A receptor signaling in mice" @default.
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• W1561724648 doi "https://doi.org/10.1016/j.ejphar.2015.05.048" @default.
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