Fas Receptor and Neuronal Cell Death after Spinal Cord Ischemia

摘要: Cell death from spinal cord injury is mediated in part by apoptotic mechanisms involving downstream caspases (e.g., caspase-3). Upstream may involve other such as procaspase-8, a 55 kDa apical caspase, which we found constitutively expressed within neurons along with Fas. As early 1.5 hr after transient ischemia, activated caspase-8 (p18) and mRNA appeared intermediate gray matter medial ventral horn. We also detected evidence for an increase receptor complex co-immunoprecipitation using Fas anti-procaspase-8 ischemia. At time points, p18 were co-expressed individual neurons, caspase-3. Moreover, cells before procaspase-3 cleavage product (p20), suggesting sequential activation. The appearance of cytosolic cytochrome c gelsolin ischemia was consistent mitochondrial release caspase-3 activation, respectively. Numerous terminal deoxynucleotidyl transferase-mediated DNA nick end-labeling-positive contained or p20 (65 80%, respectively), thereby supporting the idea that undergoing cell contain both processed caspases. Our data are induces formation death-inducing signaling complex, participate activation cleavage. Death receptors well be useful therapeutic targets limiting cord.