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- Title
JNK signaling plays an important role in the effects of TNF-α and IL-1β on in vitro osteoblastic differentiation of cultured human periosteal-derived cells.
- Authors
Hah, Young-Sool; Kang, Hea-Gea; Cho, Hee-Young; Shin, Sang-Hoon; Kim, Uk-Kyu; Park, Bong-Wook; Lee, Sang-il; Rho, Gyu-Jin; Kim, Jong-Ryoul; Byun, June-Ho
- Abstract
The purpose of this study was to examine the effects of TNF-α and IL-1β on in vitro osteoblastic differentiation of cultured human periosteal-derived cells. To examine the effects of TNF-α and IL-1β on in vitro osteoblastic differentiation of cultured human periosteal-derived cells, the cells cultured in the osteogenic induction medium were treated with 0.1-10 ng/ml TNF-α and 0.01-1 ng/ml IL-1β. TNF-α and IL-1β enhanced the alkaline phosphatase (ALP) activity and alizarin red S staining in cultured human periosteal-derived cells. However, these cytokines did not stimulate the Runt-related transcription factor (Runx) 2 activity and osteocalcin secretion. The ALP activity was decreased in the periosteal-derived cells pretreated with mitogen activated protein kinase (MAPK) inhibitors and then treated with TNF-α or IL-1β. Among the periosteal-derived cells pretreated with MAPK inhibitors, the ALP activity was markedly decreased in the cells pretreated with SP 600125, the specific inhibitor of C-Jun N-terminal kinase (JNK). The periosteal-derived cells treated with TNF-α and IL-1β showed an increase in extracellular signal-regulated kinase (ERK) and JNK phosphorylation. Among the ERK and JNK phosphorylation, JNK phosphorylation was strongly observed in the cells. These results suggest that TNF-α and IL-1β increased the in vitro osteoblastic differentiation of cultured human periosteal-derived cells by enhancing the ALP activity and mineralization process, but not by Runx2 activation. The functional role of TNF-α and IL-1β in increasing the ALP activity and mineralization of periosteal-derived cells primarily depends on the JNK signaling among the MAPK pathways.
- Publication
Molecular biology reports, 2013, Vol 40, Issue 8, p4869
- ISSN
1573-4978
- Publication type
Journal Article
- DOI
10.1007/s11033-013-2586-3