Apoptosis in Caspase-inhibited Neurons

• DOI: 10.1007/bf03401837
• Publication Date: 2018-08-31T13:57:28Z
• Authors: Christiane Volbracht; Marcel Leist; Stefan A. Kolb; Pierluigi Nicotera
• Keywords: Colchicine; Intrinsic apoptosis

There is growing evidence of apoptosis in neurodegenerative disease. However, it still unclear whether the pathological manifestations observed slow diseases are due to neuronal loss or they related independent degenerative events axodendritic network. It also remains elusive a single, caspase-based executing system involving caspases responsible for by apoptosis. Long-term exposure microtubule-disassembling agent, colchicine, was used disrupt network and eventually trigger caspase-3-mediated cultures cerebellar granule cells. For this model, we investigated role Bcl-2 neurite degeneration death somata. Early occurred caspase-independent mechanism. Conversely, cell body delayed initially blocked caspase inhibition. when activity entirely zVAD-fmk, colchicine-exposed neurons underwent characterized cytochrome c release, chromatin condensation irregularly shaped clumps, DNA-fragmentation, phosphatidylserine. Inhibitors proteasome reduced these apoptotic-like features soma. Our data suggest that Bcl-2-dependent caspase-mediated programs account only partially changes injured neurons. Blockage execution machinery may temporarily rescue damaged classical apoptotic can appear caspase-inhibited