التفاصيل البيبلوغرافية
| العنوان: |
Nectandrin A Enhances the BMP-Induced Osteoblastic Differentiation and Mineralization by Activation of p38 MAPK-Smad Signaling Pathway. |
| المؤلفون: |
Do Yeon Kim1, Go Woon Kim1, Sung Hyun Chung1 suchung@khu.ac.kr |
| المصدر: |
Korean Journal of Physiology & Pharmacology. Oct2013, Vol. 17 Issue 5, p447-453. 7p. |
| مصطلحات موضوعية: |
*OSTEOBLASTS, *MITOGEN-activated protein kinase phosphatases, *ALKALINE phosphatase, *LUCIFERASES, *MITOGEN-activated protein kinases |
| مستخلص: |
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. [ABSTRACT FROM AUTHOR] |
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