Identification of effector molecules for cellular stress and related molecular signaling pathways in chondrocyte

2014 Fiscal Year Final Research Report

• Project/Area Number: 24791572
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Orthopaedic surgery
• Research Institution: Kinki University
• Principal Investigator: ONODERA Yuta 近畿大学, 医学部附属病院, 助手 (30510911)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 変形性膝関節症 / 炎症 / Nrf2 / TAK1 / ROS / ヒアルロン酸

Outline of Final Research Achievements

My purpose of this study is to declare the molecular mechanism of catabolic action in chondrocytes/synovial cells and relationship with some stress factors. We demonstrated here that 1) Rho-ROCK signaling cascade could be a primary molecules response to mechanical stress and lead to downstream catabolic actions, 2) in the synovial cells, TAK1 is an effector molecule in the ROS-induced Cox-2 expression, and 3) hyaluronic acid (HA), which is a well known pharmacological molecules for osteoarthritis, could reduce cellular superoxide generation and accumulation via induction of overexpression of Nuclear factor-erythroid-2-related factor 2 (Nrf2), which is a master transcription factor in cellular redox reactions, in cultured chondrocyte derived from bovine joint cartilage. These studies suggest some novel mechanisms relate to responsible molecules in the stress response and activation of catabolic reactions, and its pharmacological moderator.

Free Research Field

再生医療