JNK MAPK is involved in BMP-2-induced odontoblastic differentiation of human dental pulp cells. (June 2014)

• Record Type: Journal Article
• Authors: Qin, Wei; Liu, Pengcheng; Zhang, Rong; Huang, Shuheng; Gao, Xianling; Song, Zhi; Wang, Runfu; Chen, Lingling; Guo, Bing; Lin, Zhengmei
• Is Part Of: Connective tissue research. Volume 55:Number 3(2014:Jun.)
• Page Start: 217
• Page End: 224
• Publication Date: 2014-06
• Subjects: Connective tissues -- Periodicals; 616.770072
• DOI: 10.3109/03008207.2014.882331
• Languages: English
• ISSNs: 0300-8207

Abstract

<abstract> <title>Abstract</title> <p>Bone morphogenetic protein-2 (BMP-2) is a multi-functional growth factor belonging to the transforming growth factor β superfamily that has a broad range of activities that affect many different cell types. BMP-2 induces odontoblastic differentiation of human dental pulp cells (DPCs), but the underlying mechanism remains unclear. In this study, we investigated the potential role of the JNK mitogen-activated protein kinases (MAPK) pathway in BMP-2-induced odontoblastic differentiation of DPCs. The levels of phosphorylated and unphosphorylated JNK MAPK were quantified by Western blot analysis following treatment with BMP-2 and the JNK inhibitor SP600125. The role of JNK MAPK in the BMP-2-induced odontoblastic differentiation of DPCs was determined by measuring alkaline phosphatase (ALP) activity and by examining the expression of odontoblastic markers using quantitative real-time polymerase chain reaction analysis. The effect of JNK MAPK silencing on odontoblastic differentiation was also investigated. BMP-2 upregulated the phosphorylation of JNK in DPCs in a dose- and time-dependent manner. Early markers of odontoblastic differentiation, including ALP activity, osteopontin and dentin matrix protein-1, were not inhibited by the JNK inhibitor. However, the JNK inhibitor, SP600125, significantly inhibited late-stage differentiation of odontoblasts, including the gene expression of osteocalcin, dentin sialophosphoprotein and bone sialoprotein, and also reduced the formation of mineralized nodules in BMP-2-treated DPCs. Consistent with this observation, silencing of JNK MAPK also decreased late-stage odontoblastic differentiation. Taken together, these findings suggest that JNK activity is required for late-stage odontoblastic differentiation induced by BMP-2.</p> </abstract>