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Updated: May 17, 2026
Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Traumatic brain injury induces a downregulation of MSK1 in rat brain cortex
1Department of Neurosurgery, Shandong Provincial Hospital, Shandong University, Jinan, 250012, People's Republic of China. ningbo197410@163.com
Abstract:
Mitogen- and stress-activated protein kinase (MSK) 1 protein was initially identified as a particularly interesting protein of mitogen-activated protein kinase. It was reported to enhance B cell lymphoma 2-associated death protein's phosphorylation to protect cell death, suggesting that MSK1 represents a new type of anti-cell death gene. Moreover, a recent study has shown that MSK1 is involved in negative feedback pathways that are crucial to prevent uncontrolled inflammation. However, its function and expression in the central nervous system lesion are not been understood very well. In this study, we performed a traumatic brain injury (TBI) model in adult rats and investigated the dynamic changes of MSK1 expression in the brain cortex. Double immunofluorescence staining revealed that MSK1 was co-expressed with neuronal nuclei (NeuN) and glial fibrillary acidic protein (GFAP). Besides, co-localization of MSK1/active caspase 3 and MSK1/proliferating cell nuclear antigen (PCNA) was detected in NeuN and GFAP. We also examined the expression profiles of PCNA and active caspase 3 whose changes were correlated with the expression of MSK1. All our findings suggested that MSK1 might be involved in the pathophysiology of brain after TBI.
Insights
Mitogen- and stress-activated protein kinase 1 (MSK1) plays a role in protecting cells from death and regulating inflammation. This study investigates MSK1 expression in traumatic brain injury (TBI) models, suggesting its involvement in brain injury pathophysiology.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Mitogen- and stress-activated protein kinase 1 (MSK1) is known for its anti-apoptotic and anti-inflammatory roles.
- Its function and expression within the central nervous system, particularly after injury, remain largely uncharacterized.
Purpose of the Study:
- To investigate the dynamic changes and cellular localization of MSK1 in the adult rat brain following traumatic brain injury (TBI).
- To explore the relationship between MSK1 expression and markers of cell death and proliferation in the injured brain.
Main Methods:
- Establishment of a rat model of traumatic brain injury (TBI).
- Analysis of MSK1 expression using double immunofluorescence staining in brain cortex tissue.
- Co-localization studies with neuronal marker NeuN, astrocyte marker GFAP, proliferation marker PCNA, and apoptosis marker active caspase 3.
Main Results:
- MSK1 expression was detected in both neurons (NeuN+) and astrocytes (GFAP+) in the TBI model.
- Co-localization of MSK1 with active caspase 3 and PCNA was observed in neurons and astrocytes.
- Changes in PCNA and active caspase 3 expression correlated with MSK1 expression levels.
Conclusions:
- MSK1 is expressed in neurons and astrocytes in the brain cortex after TBI.
- The findings suggest that MSK1 is involved in the cellular responses, including proliferation and apoptosis, following traumatic brain injury.
- MSK1 may play a significant role in the pathophysiology of brain injury.
