2013 Fiscal Year Final Research Report
Analysis of the role of mechanosensor-mediated JNK/p38 signaling in osteoimmunological regulation of osteoblasts
| Project/Area Number |
24792059
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Prosthetic dentistry
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Keywords | メカノバイオロジー / 骨代謝 / JNK / p38 |
|---|
| Research Abstract |
In this study, we report that large-magnitude (12%) cyclic stretch induced Ca2+ influx in MC3T3-E1 osteoblasts, which subsequently activated ASK1 MAP3K. The activated ASK1-JNK lead to transiently enhanced expression of FGF-inducible 14 (Fn14, a member of the TNF receptor superfamily) gene. Cells with enhanced expression of Fn14 subsequently acquired sensitivity to the ligand of Fn14, TNF-related weak inducer of apoptosis, and underwent apoptosis. On the other hand, ASK1-p38 pathway induced expression of monocyte chemoattractant protein-3 (MCP-3) gene, which promoted chemotaxis of pre-osteoclasts. These results suggest that ASK1-JNK/p38 pathways contribute to the mechanism of mechanical overloading-induced bone resroption via cytokine-related gene expression.
|
-
[Journal Article] The expression of Fn14 via mechannical stress-activated JNK contributes to apoptosis induction in osteoblasts2014
Author(s)
Matsui H., Fukuno N., Kanda Y., Kantoh Y., Chida T., Nagaura Y., Suzuki O., Nishitoh H., Takeda K., Ichijo H., Sawada Y., Sasaki K., Kobayashi T., and Tamura S
-
Journal Title
J. Biol. Chem
Volume: 289
Pages: 6438-6450
Peer Reviewed
-
-
-
-
