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Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
Published on: August 7, 2018
Nemo-like kinase (NLK) involves in neuronal apoptosis after traumatic brain injury
Zhen Li1, Gang Cui, Junxiang Wang
1Neurosurgery of the Central Hospital of TaiAN, TaiAN, China.
Abstract:
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.
Insights
Nemo-like kinase (NLK) is down-regulated in traumatic brain injury (TBI), correlating with increased caspase-3. This suggests NLK may play a role in TBI-induced neuronal apoptosis.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Traumatic brain injury (TBI) involves immediate mechanical damage and a delayed phase of biochemical events leading to neuronal cell death.
- The molecular mechanisms underlying delayed neuronal apoptosis after TBI remain poorly understood.
- Nemo-like kinase (NLK), a serine/threonine kinase, is implicated in neuronal apoptosis.
Purpose of the Study:
- To investigate the role of nemo-like kinase (NLK) in neuronal apoptosis following traumatic brain injury (TBI).
- To explore the relationship between NLK expression and caspase-3 activity in the context of TBI.
Main Methods:
- Western blot analysis to assess protein levels of NLK and caspase-3.
- Double immunofluorescent staining and immunohistochemistry to analyze NLK's role in TBI models.
- CCK-8, western blot, and TUNEL assays to evaluate the effect of NLK overexpression on PC12 cell apoptosis induced by glutamate.
Main Results:
- Significant down-regulation of NLK was observed during the early stage of TBI.
- A concomitant up-regulation of caspase-3 was detected concurrently with NLK down-regulation.
- Overexpression of NLK in PC12 cells reduced glutamate-induced apoptosis.
Conclusions:
- NLK expression is reduced following TBI, coinciding with increased caspase-3 activity.
- NLK may be involved in the down-regulation of caspase-3 expression after TBI.
- These findings suggest NLK plays a protective role against TBI-induced neuronal apoptosis.
