Upregulation of BNIP3 and translocation to mitochondria in nutrition deprivation induced apoptosis in nucleus pulposus cells

ObjectiveThis 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.MethodsCells 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.ResultCell 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 72 h. Furthermore, the protein was found to translocate to mitochondria.ConclusionUpregulation 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.