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KMID : 0811720130170050447
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Korean Journal of Physiology & Pharmacology
2013 Volume.17 No. 5 p.447 ~ p.453
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Nectandrin A Enhances the BMP-Induced Osteoblastic Differen-tiation and Mineralization by Activation of p38 MAPK-Smad Sig-naling Pathway
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Kim Do-Yeon
Kim Go-Woon
Chung Sung-Hyun
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Abstract
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Osteoblastic activity of nectandrin A was examined in C2C12 cells. Nectandrin A enhances the BMP-induced osteoblastic differentiation and mineralization, manifested by the up-regulation of differentiation markers (alkaline phosphatase and osteogenic genes) and increased calcium contents. In C2C12 cells co-transfected with expression vector encoding Smad4 and Id1-Luc reporter, nectandrin A increased Id1 luciferase activity in a concentration-dependent manner, when compared to that in BMP-2 treated cells, indicating that Smad signaling pathway is associated with nectandrin A-enhanced osteoblastic differentiation in C2C12 cells. In addition, nectandrin A activated p38 mitogen-activated protein kinase (MAPK) in time- and concentration-dependent manners, and phosphorylated form of pSmad1/5/8 and alkaline phosphatase activity were both decreased when the cells were pretreated with SB203580, a p38 MAPK inhibitor, suggesting that p38 MAPK might be an upstream kinase for Smad signaling pathway. Taken together, nectandrin A enhances the BMP-induced osteoblastic differentiation and mineralization of C2C12 cells via activation of p38 MAPK-Smad signaling pathway, and it has a therapeutic potential for osteoporosis by promoting bone formation.
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KEYWORD
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C2C12, Nectandrin A, p38 MAPK, Smad
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