Overexpression of BNIP3 in rat intervertebral disk cells triggers autophagy and apoptosis

Excessive apoptosis of intervertebral disk cells and degeneration (IDD) is the prime cause low back pain. B-cell lymphoma 2 (Bcl-2) adenovirus E1B 19 kDa interacting protein 3 (BNIP3), a member Bcl-2 family, are involved in cell autophagy apoptosis. The roles mechanisms BNIP3 unclear. In this study, primary rat were prepared to study effect overexpression on their counting kit (CCK)-8 assay showed that decreased viability. Real-time PCR Western blotting significantly upregulated expression autophagy-related proteins pro-apoptotic proteins, including hypoxia-inducible factor-1?, apoptotic protease activating factor 1, caspase cleaved 3, microtubule-associated 1A/1B light chain (LC3) Beclin-1 while downregulating anti-apoptotic Bcl-2. Cell staining detection increased cells. RNA interference revealed effects can be reversed. These findings suggested enhanced vitro, which might promote IDD development.