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Acta Biochimica et Biophysica Sinica Advance Access originally published online on October 13, 2009
Acta Biochimica et Biophysica Sinica 2009 41(11):938-947; doi:10.1093/abbs/gmp087
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© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

Double role of Fas ligand in the apoptosis of intervertebral disc cells in vitro

Dunfu Han1,{dagger}, Yue Ding1,{dagger}, Shang-Li Liu1,*, Gang Wang1, In-Cheong Si1, Xinguang Wang1, Liyang Cui1,2 and Dongshang Huang1

1 Department of Orthopaedic Surgery, The Second Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510120, China
2 Department of Orthopedic Surgery, The People's Hospital of Henan Province, Zhengzhou 450003, China

* Correspondence address. Tel: +86-20-34071151; Fax: +86-20-81867705; E-mail: gzxy168{at}126.com


  Abstract

Fas ligand (FasL) may play an important role in maintaining the immune privilege of intervertebral disc (IVD). Besides, it is closely related to the apoptosis of degenerative disc cells. Nowadays, lots of reports have described about the paradoxical effects of FasL, although the effect of FasL on IVD cells is still under debate. In this study, we tried to investigate the effects of FasL on Fas expression and on the apoptosis of nucleus pulposus (NP) cells in Sprague–Dawley rats. The results showed that the expression of Fas in NP cells was significantly increased by the recombinant FasL. Meanwhile, the apoptosis of NP cells increased markedly in a FasL dose-dependent manner. Interestingly, RNA interference results indicated that the increase of Fas expression and the NP cell apoptosis described previously were inhibited by Fas siRNA, suggesting that RNA interference might be one of novel strategies to prevent IVD cells from apoptosis.

Keywords    apoptosis; Fas; Fas ligand; intervertebral disc; RNA interference

Received: March 17, 2009; Accepted: July 3, 2009

{dagger} These authors contributed equally to this work.


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