Traumatic brain injury induces a downregulation of MSK1 in rat brain cortex.

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.

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