2017 Fiscal Year Final Research Report
Development of the model of wound healing mechanism using TIMP1 and HIF
| Project/Area Number |
16K20453
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Conservative dentistry
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
OKAMOTO MOTOKI 大阪大学, 歯学部附属病院, 医員 (60755354)
|
|---|
| Research Collaborator |
MANAHILALI SAEED
WATANABE MASAKATU
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Keywords | 歯学 / 覆髄 / 象牙質 / 歯髄 / 再生 |
|---|
| Outline of Final Research Achievements |
Tissue Inhibiter of metaroprotease 1(TIMP1) can be worked as inhibiter against MMP which play acentral role in the degradation of extracellular matrix.Addtionaly,TIMP1 were found to promoted the various function of pulpal cells in vitro and also induced tertiary dentin in pulp tissue in vivo. As a mechanism of wound healing with TIMP1,a group of genes regulated by HIF1α was candidate. Therefore, DFO was applied as direct pulp capping. DFO also induced tertiary dentin similar to TIMP1 and ProRoot MTA.
These effect were inhibited by administration of rapamycin. Rapamycin was consider as inhibiter as mTOR and HIF. From these result, mTOR and HIF play important role of wound healing process in dentin pulp complex.And, TIMP1 and DFO had possibilities to development of true biological pulp capping materials.
|
| Free Research Field |
保存治療系歯学
|
