The study of endoplasmic reticulum stress pathway in mechanical stress-loaded chondrocyte

2016 Fiscal Year Final Research Report

• Project/Area Number: 26462303
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Orthopaedic surgery
• Research Institution: Kumamoto University
• Principal Investigator: Mizuta Hiroshi 熊本大学, 大学院生命科学研究部(医), 教授 (60174025)
• Co-Investigator(Renkei-kenkyūsha): OYADOMARI Seiichi 徳島大学, 疾患ゲノム研究センター, 教授 (90502534)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 小胞体ストレス / 軟骨細胞機能 / アポトーシス

Outline of Final Research Achievements

This study showed that endoplasmic reticulum (ER) stress was induced by long-term excessive mechanical stress, resulting decrease of anabolic function, increase of catabolic function, and apoptosis in cultured chondrocytes. We also confirmed this finding in conditions mimicking the intra-articular environments in elderly patients with osteoarthritis. Furthermore, it was suggested that ATF6α, the ER stress sensor protein, may reduce the negative effects by mechanical stress such as decrease of anabolic function, increase of catabolic function, and increase of apoptosis in chondrocytes.

Free Research Field

整形外科