Bcl-2 protein inhibits oxysterol-induced apoptosis through suppressing CPP32-mediated pathway
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Updated: Nov 1, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles
Published on: October 5, 2012
K Harada1, S Ishibashi, T Miyashita
1Third Department of Internal Medicine, University of Tokyo, Bunkyo-Ku, Japan.
Abstract:
Oxysterols are presumed to mediate cytotoxicity of oxidized LDL in atherosclerotic lesions. To elucidate its molecular mechanism, we established murine macrophage-like P388-D1 cells which over-express Bcl-2 protein by retrovirus-mediated gene transfer. Oxysterols (7-ketocholesterol, 25-hydroxycholesterol) induced nuclear condensation and oligonucleosomal DNA fragmentation, which were partially inhibited by Bcl-2 over-expression. Though CPP32 inhibitor suppressed the cell death in control cells, it showed no additive protection in the cells over-expressing Bcl-2. These findings indicate that oxysterols induce apoptosis via Bcl-2-inhibitable and -uninhibitable pathways, and the former depends on CPP32 activation.
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