Project/Area Number |
25462952
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Conservative dentistry
|
Research Institution | Niigata University |
Principal Investigator |
YOSHIBA NAGAKO 新潟大学, 医歯学総合病院, 講師 (10323974)
|
Co-Investigator(Kenkyū-buntansha) |
YOSHIBA KUNIHIKO 新潟大学, 医歯学系, 准教授 (30220718)
OHKURA NAOTO 新潟大学, 医歯学総合病院, 医員 (00547573)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | α-SMA / fibrillin-1 / dental pulp / organ culture / 歯髄組織 / myofibroblast / culture / TGF-β1 / pSmad2/3 / alpha-SMA / pulp tissue |
Outline of Final Research Achievements |
Alpha-smooth muscle actin (α-SMA) is a marker of myofibroblasts, which play a central role in wound healing. Fibrillin-1 is a major constituent of microfibrils and an extracellular-regulator of TGF-β1, an important cytokine for myofibroblasts differentiation. We examined alterations of α-SMA and fibrillin-1 expression in organotypic culture of dental pulp. After 7 days of culture, most fibroblasts and odontoblasts were immunoreactive for α-SMA with a significant increase of α-SMA mRNA expression. Furthermore, immunostaining of fibrillin-1 became faint with mRNA downregulation. Administration of inhibitors for extracellular matrix proteases resulted in the recovery of fibrillin-1 immunostaining, and fibroblasts lost their immunoreactivity for α-SMA with mRNA downregulation. These findings suggest that fibrillin-1 degradation and downregulation might be implicated in the myofibroblasts differentiation in dental pulp wound healing.
|