Project/Area Number |
24592196
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Orthopaedic surgery
|
Research Institution | Kobe University |
Principal Investigator |
MAENO Koichiro 神戸大学, 医学(系)研究科(研究院), 助教 (70403269)
|
Co-Investigator(Kenkyū-buntansha) |
NISHIDA Kotaro 神戸大学, 医学部附属病院, 講師 (00379372)
KAKUTANI Kenichiro 神戸大学, 医学部附属病院, 助教 (10533739)
DOITA Minoru 神戸大学, 大学院医学研究科, 医学研究員 (60237170)
|
Research Collaborator |
YAMAMOTO Junya 神戸大学, 大学院医学研究科
HIRATA Hiroaki 神戸大学, 大学院医学研究科
KURAKAWA Takuto 神戸大学, 大学院医学研究科
TERASHIMA Yoshiki 神戸大学, 大学院医学研究科
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 椎間板 / Fas ligand / ADAM10 / マクロファージ / 炎症性サイトカイン / adiponectin / 硬膜外脂肪 / 変性 / 硬膜外脂肪組織 / 抗炎症作用 / 創外固定型モデル / 脊索由来細胞 / Fas / 共培養 / reverse signaling |
Outline of Final Research Achievements |
The production of pro-inflammatory cytokines was found to be far larger at the co-culture group that was cultured with macrophages and Fas Ligand (FasL) overexpressed intervertebral nucleus pulposus cells. Furthermore, it was found that the expression of ADAM (A Disintegrin And Metalloproteinase) 10, which controls the expression of FasL, was also increased. And also, mRNA expression of TNF-α was significantly increased stimulating by IL-1β+adiponectin. From these results, we consider that FasL and ADAM10 play an important role in the production of pro-inflammatory cytokines coming from interaction of the intervertebral nucleus pulposus cells and macrophages. Also, the adiponectin which is an adipocyte specific hormone known to have anti-diabetic, anti-atherogenic and anti-inflammatory effects, may have inhibited permanently inflammatory reaction around the intervertebral disc.
|