Pathogenesis and pathological role of endoplasmic reticulum stress in cartilage degeneration
Project/Area Number |
20591784
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Orthopaedic surgery
|
Research Institution | Kumamoto University |
Principal Investigator |
MIZUTA Hiroshi Kumamoto University, 大学院・生命科学研究部, 教授 (60174025)
|
Co-Investigator(Kenkyū-buntansha) |
HIROSE Jun 熊本大学, 医学部附属病院, 講師 (40433007)
SENBA Kei 熊本大学, 医学部附属病院, 医員 (00398190)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 糖化最終産物 / 小胞体ストレス / アポトーシス / 細胞・組織 / シグナル伝達 / ストレス / 小胞体 |
Research Abstract |
Endoplasmic reticulum stress (ER stress) induced by intracellular advanced glycation end products (AGEs) caused chondrocyte dysfunction and apoptosis in vitro and in vivo study of rats. Human osteoarthritic chondrocytes were more sensitive to AGEs-induced ER stress than normal chondrocytes. These pathological responses are recognized as a new mechanism of the cartilage degeneration.
|
Report
(4 results)
Research Products
(8 results)