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Joint Bone Spine
Volume 79, n° 2
pages 186-191 (mars 2012)
Doi : 10.1016/j.jbspin.2011.04.011
accepted : 19 April 2011
Upregulation of BNIP3 and translocation to mitochondria in nutrition deprivation induced apoptosis in nucleus pulposus cells

Jie Liu 1, Jian Wang 1, Yue Zhou
Department of Orthopaedics, XinQiao Hospital, The Third Military Medical University, Chongqing 400038, PR China 

Corresponding author. Tel.: +86 236 877 4608; fax: +86 236 877 4608.

This study was to detect the expression of Bcl-2/adenovirus E1B19-kDa-interacting protein 3 in apoptosis induced by nutrition deprivation in nucleus pulposus cells, so as to further understand the mechanism of apoptosis in nucleus pulposus cells.


Cells isolated from rat caudal disc were cultured under two different oxygen, glucose and serum concentrations for up to 3 days. Interactions between two different concentrations were examined by cell vitality assay mitochondrial membrane potential (Δψm ) test and apoptosis detect. The expression and location of Bcl-2/adenovirus E1B19-kDa-interacting protein 3 were tested by real-time polymerase chain reaction and immunofluorescence staining.


Cell vitality and mitochondrial membrane potential (Δψm ) were significantly reduced in absence of oxygen, glucose and serum while the cell apoptosis percent was significantly increased, as compared with the cells in normal oxygen, glucose and serum concentration. The expression of Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 showed a significant increase in absence of oxygen, glucose and serum, especially in 72h. Furthermore, the protein was found to translocate to mitochondria.


Upregulation of Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 and translocation to mitochondria may be involved in apoptosis of nucleus pulposus cells in nutrition deprivation.

The full text of this article is available in PDF format.

Keywords : Nucleus pulposus cells, Bcl-2/adenovirus E1B 19-kDa-interacting protein 3, Mitochondria, Nutrition deprivation

1  Dr. Jie Liu and Dr. Jian Wang did the equal contribution for this research.

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