2013 Fiscal Year Final Research Report

Caspase 3 Silencing Inhibits Biomechanical Overload-induced Intervertebral Disc Degeneration

Research Project

Project/Area Number	23592150
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Orthopaedic surgery
Research Institution	Hokkaido University
Principal Investigator	SUDO HIDEKI 北海道大学, 医学(系)研究科(研究院), 特任准教授 (30374367)
Project Period (FY)	2011 – 2013
Keywords	アポトーシス / 椎間板 / 変性制御
Research Abstract	Intervertebral disc (IVD) degeneration causes debilitating low back pain in large sections of the worldwide population. No efficient treatment currently exists because the unclear pathogenesis. One characteristic event early in the degeneration is the apoptosis of nucleus pulposus (NP) cells embedded in IVD. Excessive biomechanical loading may be also a major etiology of IVD degeneration. The present study used in vitro and in vivo models of compressive loading to elucidate the underlying mechanism of IVD degeneration. In addition, we investigated whether the inhibition of apoptosis is a potential clinical therapeutic strategy for the treatment of IVD degeneration induced by biomechanical stress.The present study suggests that caspase 3 siRNA attenuates overload-induced IVD degeneration by inhibiting NP cell apoptosis and the expression of matrix-degrading enzymes.