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Title: Vanillic acid exerts oestrogen-like activities in osteoblast-like UMR 106 cells through MAP kinase (MEK/ERK)-mediated ER signaling pathway
Authors: Xiao, HH
Gao, QG
Zhang, Y
Wong, KC
Dai, Y
Yao, XS
Wong, MS 
Keywords: Vanillic acid
Phenolic acid
MAP kinase mediated pathway
Sambucus williamsii Hance
Issue Date: 2014
Publisher: Pergamon Press
Source: Journal of steroid biochemistry and molecular biology, 2014, v. 144, p. 382-391 How to cite?
Journal: Journal of steroid biochemistry and molecular biology 
Abstract: Sambucus williamsii Hance (SWH) has been used for treatment of bone and joint disease in China for thousands of years. Our previous study showed that SWH extract and its bioactive fraction could effectively prevent oestrogen-deficiency induced bone loss in ovariectomized mice. The present study aimed to study the bone protective effects of vanillic acid (VA), a phenolic acid isolated from the bioactive fraction of SWH, and to characterize the signaling pathways that mediated its actions in rat osteoblast-like UMR 106 cells. VA significantly stimulated proliferation, alkaline phosphatase (ALP) activities as well as significantly altered the mRNA expression of genes involved in osteoblast functions and osteoclastogenesis in UMR 106 cells. Co-treatment of UMR 106 cells with 10(-6) M ICI182,780 (a specific oestrogen receptor (ER) antagonist) abolished the stimulatory effects of VA on osteoblast proliferation and ALP activities, suggesting the role of ER in mediating its actions. However, VA (10(-12) to 10(-6) M) failed to bind to ER alpha or ER beta and did not activate oestrogen response element (ERE)-luciferase activities via ER alpha or ER beta in UMR 106 cells. In contrast, 10(-10) and 10(-8) M of VA induced the phosphorylation of MEK 1/2, ERK1/2 and ERa at Ser118 residue in UMR 106 cells, suggesting that MAP kinase-mediated pathway is involved in mediating its actions. Taken together, our results indicated that VA is a bioactive compound in SWH that exerts stimulatory effects in osteoblast-like cells via non-genomic, but not classical, ER signaling pathway.
ISSN: 0960-0760
DOI: 10.1016/j.jsbmb.2014.08.002
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