Nemo-like kinase (NLK) involves in neuronal apoptosis after traumatic brain injury.

Traumatic brain injury (TBI) consists of two phases: an immediate phase in which damage is caused as a direct result of the mechanical impact: and a late phase of altered biochemical events that results in delayed tissue damage and is therefore amenable to therapeutic treatment. Because the molecular mechanisms of delayed post-traumatic neuronal cell death are still poorly understood, we investigated whether nemo-like kinase (NLK), an evolutionarily conserved serine/threonine kinase involved in neuronal apoptosis following TBI. In the model of TBI, western blot analysis, double immunofluorescent staining and immunohistochemistry were used to analyze the role of NLK in the process. The results showed a significant down-regulation of NLK and a concomitant up-regulation of caspase-3 during the early stage of TBI. In the model of glutamate inducing PC12 apoptosis, we analyzed the effect of over-expression of NLK on the neuronal cell line PC12 apoptosis by cck-8, western blot and TUNEL assays. Together with previous reports. We hypothesize NLK was related to the down-regulation of caspase-3 expression after TBI, and such an event may be associated with neuronal apoptosis.