• Naoki Otani, Hiroshi Nawashiro, Shinji Fukui, Namiko Nomura, and Katsuji Shima.
• Department of Neurosurgery, National Defense Medical College, Tokorozawa, Japan. grd1405@gr.ndmc.ac.jp
• J. Neurotrauma. 2002 Dec 1;19(12):1587-96.

AbstractMitogen-activated protein kinases (MAPK) play a crucial role in signal transduction that regulates gene expression through transcriptional factor activity. The purpose of this study was to investigate the temporal expression and topographic distribution of the activated MAPK pathways including extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), and p38 MAPK following traumatic brain injury (TBI) in the cortex of the rat brain. Adult male Sprague-Dawley rats (300-400 g) were subjected to lateral fluid percussion injury of moderate severity (3.5-4.0 atm) using the Dragonfly device model (no. HPD-1700). Phosphorylated-MAPK protein levels were quantified using Western blot analysis. Topographic distribution of immunoreactivity for phosphorylated-MAPK was examined using immunohistochemistry. Our findings showed that TBI significantly increased the phosphorylated-ERK (p-ERK) and -JNK (p-JNK) levels, but not the -p38 (p-p38) protein levels in the cortex surrounding the injury site. The immunoreactivity for p-ERK and p-JNK immediately after TBI were localized in neurons. The immunoreactivity for p-JNK was uniformly but only transiently induced and returned to control levels 1 h after TBI. The immunoreactivity for p-ERK was confirmed up until 30 min after TBI in the superficial neuronal layers. Double immunostaining using a glial-specific marker demonstrated that p-ERK was prominent in astrocytes 6 h after TBI. The current results suggest that the ERK and JNK pathways, but not the p38 MAPK pathways are involved in signal transduction in the cortex following TBI.

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