Our results revealed that the expression of the members of NT family (Nerve-Growth Factor (NGF), Brain-Derived Neurotrophic Factor (BDNF), and Neurotrophin-3 (NT-3)) is significantly declined in the injured spinal cord,
as early as 6 h after the induction of the contusion. The expression was recovered afterward to that of the control levels. Furthermore, the expression of all NTs high-affinity Trk receptors decreased severely after the contusion. While the expression of TrkA and TrkC were completely shut down after 6 and 12 h after injury respectively, the expression of TrkB receptor declined at 12 h after injury and remained at this low level thereafter. In contrast to the pattern of Trk receptor expression, p75NTR receptor showed a significant upregulation after contusion. The expression of PC members functioning in the constitutive secretory pathway, i.e.
furin, PACE4 and PC7, increased after Nepicastat molecular weight damage, while the expression of PC members acting in regulated secretory pathway, PC1 and PC2, reduced after spinal cord injury. All together, the down-regulation of NTs, their designated Trk receptors and PC1/PC2 enzymes along with an upregulation of p75NTR promote neuronal death after injury. Our results suggest that either overexpression of NTs, Trk receptors and PC1/PC2 or interfering with the expression of p75NTR see more in host and/or grafted cells before transplantation could increase the success of the transplantation. (c) 2008 Elsevier Ireland Ltd. Ali rights reserved.”
“The mechanism by which a brief episode of sublethal ischemia followed by reperfusion (ischemic preconditioning, IPC) prevents the lethal effects of subsequent periods of prolonged ischemia, are poorly understood. A completely randomized, controlled study was designed to study the effect of IPC using a rabbit model of ischemic spinal
cord injury. Twenty-four white adult New England rabbits were randomly assigned to one of 3 groups (n = 8 per group); the groups were assigned as follows: Group I: sham-operation group, Group II: ischemic reperfusion MEK162 mw (I/R) group, and Group III: ischemic preconditioning group. Spinal cord ischemia was induced by introducing an infra renal aortic cross-clamp for 30 min. Following injury, rabbits were subjected to 30 min, 2 h, or 8 h of reperfusion in Group II. In Group III, subjects underwent three cycles, 5 min each, of ischemia followed by 5 min of reperfusion, before receiving 30 min of ischemia. We previously reported that the association between ASK1 (apoptosis signal-regulating kinase 1) and 14-3-3 played an important role in regulating ischemia)reperfusion spinal cord injuries. To evaluate the effect of ischemic preconditioning in injured spinal cords, we examined alterations in spinal tissue morphology, activation of key members of the ASK1-mediated signaling pathway, and the association between ASK1 and 14-3-3.