Impairment of the mitochondrial respiratory enzyme activity triggers sequential activation of apoptosis‐inducing factor‐dependent and caspase‐dependent signaling pathways to induce apoptosis after spinal cord injury

• DOI: 10.1111/j.1471-4159.2006.04445.x
• Publication Date: 2007-02-10T10:43:24Z
• Authors: Kay L. H. Wu; Chin Hsu; Julie Y. H. Chan
• Keywords: Apoptosis-inducing factor; Mitochondrial respiratory chain

The mitochondrion participates in caspase-independent or caspase-dependent apoptotic pathways through the release of apoptosis-inducing factor cytochrome c. Whether both mitochondrial cascades are triggered injured spinal cord remains unknown. Here, we demonstrated that neurons, astrocytes and microglia segments proximal to a complete transection underwent two phases cell death. early phase high-molecular weight (HMW) DNA fragmentation was associated with nuclear translocation factor, reduction respiratory chain enzyme activity decrease cellular ATP concentration. delayed low-molecular (LMW) accompanied by cytosolic c, activation caspases 9 3, resumption functions contents. Microinfusion coenzyme Q(10), an electron carrier chain, into epicenter transected attenuated induced apoptosis, reversed elicited dysfunction, bioenergetic failure, 3. We conclude dysfunction after represents initiating events trigger sequential factor-dependent signaling cascades, leading death cord.