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Published on: September 11, 2017
Dynamic change of SGK expression and its role in neuron apoptosis after traumatic brain injury
1Department of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province 226001, People's Republic of China.
Aims:
Activation of specific signaling pathways in response to mechanical trauma causes delayed neuronal apoptosis; GSK-3β/β-catenin signaling plays a critical role in the apoptosis of neurons in CNS diseases, SGK was discovered as a regulator of GSK-3β/β-catenin pathway, The goal of this study was to determine if the mechanism of cell death or survival mediated by the SGK/GSK-3β/β-catenin pathway is involved in a rat model of TBI.
Main Methods:
Here, an acute traumatic brain injury model was applied to investigate the expression change and possible roles of SGK, Expression of SGK, and total-GSK-3β, phospho-GSK3β on ser-9, beta-catenin, and caspase-3 were examined by immunohistochemistry and Western blot analysis. Double immunofluorescent staining was used to observe the SGK localizations. Si-RNA was performed to identify whether SGK regulates neuron apoptosis via GSK-3β/β-catenin pathway, ultimately inhibit caspase-3 activation.
Key Findings:
Temporally, SGK expression showed an increase pattern after TBI and reached a peak at day 3. Spatially, SGK was widely expressed in the neuron, rarely in astrocytes and oligodendrocytes; in addition, the expression patterns of active caspase-3 and phospho-GSK3β were parallel with that of SGK, at the same time, the expression of β-catenin shows similarity with SGK. In vitro, to further investigate the function of SGK, a neuronal cell line PC12 was employed to establish an apoptosis model. We analyzed the association of SGK with apoptosis on PC12 cells by western blot, immunofluorescent labeling and siRNA.
Significance:
the results implied that SGK plays an important role in neuron apoptosis via the regulation of GSK3β/β-catenin signaling pathway; ultimately inhibit caspase-3 activation. Taken together, we inferred traumatic brain injury induced an upregulation of SGK in the central nervous system, which show a protective role in neuron apoptosis.
Insights
Serum- and glucocorticoid-regulated kinase (SGK) is upregulated after traumatic brain injury (TBI) in rats, playing a protective role in neuron apoptosis by regulating the GSK-3β/β-catenin pathway and inhibiting caspase-3 activation.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Mechanical trauma activates signaling pathways leading to delayed neuronal apoptosis.
- GSK-3β/β-catenin signaling is crucial in the apoptosis of neurons in central nervous system (CNS) diseases.
- SGK has been identified as a regulator of the GSK-3β/β-catenin pathway.
Purpose of the Study:
- To investigate the role of the SGK/GSK-3β/β-catenin pathway in neuronal cell death or survival following traumatic brain injury (TBI) in a rat model.
- To determine if SGK regulates neuron apoptosis via the GSK-3β/β-catenin pathway, ultimately inhibiting caspase-3 activation.
Main Methods:
- An acute TBI model in rats was used to examine SGK expression and its role.
- Immunohistochemistry and Western blot analysis were employed to assess the expression of SGK, GSK-3β, phospho-GSK3β, β-catenin, and caspase-3.
- Double immunofluorescent staining was used for SGK localization, and siRNA was utilized to investigate SGK's regulatory function in the pathway.
Main Results:
- SGK expression increased post-TBI, peaking at day 3, and was primarily localized in neurons.
- Expression patterns of active caspase-3 and phospho-GSK3β paralleled SGK expression, while β-catenin expression showed similarity to SGK.
- In vitro studies using PC12 cells confirmed the association between SGK and apoptosis, with siRNA demonstrating SGK's regulatory role.
Conclusions:
- SGK plays a significant role in neuron apoptosis by regulating the GSK-3β/β-catenin signaling pathway and inhibiting caspase-3 activation.
- TBI induces SGK upregulation in the CNS, suggesting a protective function against neuronal apoptosis.
