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Updated: Aug 11, 2026
Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice
Published on: August 22, 2011
Regional expression of Par-4 mRNA and protein after fluid percussion brain injury in the rat
H S Dhillon1, G X Dong, D M Yurek
1Department of Surgery, University of Kentucky Chandler Medical Center, Lexington, KY 40536, USA.
Abstract:
Regional levels of prostate apoptosis response-4 (Par-4) protein and mRNA were measured after lateral fluid percussion (FP) brain injury in rats. Immunochemical studies indicated that Par-4 immunoreactivity (ir) is present in cortical neurons and hippocampal CA1-CA3 pyramidal neurons in uninjured rats. Increases of Par-4-ir were observed in the CA3 neurons of the ipsilateral hippocampus (IH), but not in injured left cortex (IC) at 48 h after FP brain injury. Levels of the Par-4 mRNA measured by RT-PCR assay and protein measured by Western blot procedure were significantly increased in the injured IC and IH, but not in the contralateral right cortex and hippocampus after brain injury. Levels of both Par-4 protein and mRNA were significantly increased in the IC and IH as early as 2 h and stayed elevated at 24 and 48 h after injury. These data show that the induction of proapoptotic Par-4 mRNA and protein occurs only in the IC and IH that have been observed to undergo apoptosis and neuronal cell loss after lateral FP brain injury. Because increased expression of Par-4 has been observed to contribute to apoptosis and cell death in cultured neurons, the present temporal pattern of Par-4 expression is consistent with a role for Par-4 in apoptosis and neuronal cell death after traumatic brain injury.
Insights
Prostate apoptosis response-4 (Par-4) protein and mRNA increase in rat brains after injury. This finding suggests Par-4 plays a role in neuronal cell death following traumatic brain injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Prostate apoptosis response-4 (Par-4) is a pro-apoptotic protein.
- Traumatic brain injury (TBI) can lead to neuronal cell death.
- The role of Par-4 in TBI-induced neuronal apoptosis is not fully understood.
Purpose of the Study:
- To investigate the regional and temporal expression patterns of Par-4 mRNA and protein in the rat brain following lateral fluid percussion (FP) brain injury.
- To determine if Par-4 expression correlates with neuronal apoptosis and cell loss after TBI.
Main Methods:
- Rats were subjected to lateral fluid percussion (FP) brain injury.
- Par-4 protein levels were assessed using immunochemical studies and Western blot.
- Par-4 mRNA levels were quantified using RT-PCR.
- Expression was analyzed in the injured cortex and hippocampus at various time points (2, 24, and 48 hours post-injury).
Main Results:
- Par-4 immunoreactivity was observed in cortical and hippocampal neurons of uninjured rats.
- Following TBI, Par-4 mRNA and protein levels significantly increased in the injured cortex and ipsilateral hippocampus.
- These increases were observed as early as 2 hours post-injury and remained elevated at 24 and 48 hours.
- Elevated Par-4 expression was localized to regions exhibiting apoptosis and neuronal cell loss.
Conclusions:
- The induction of pro-apoptotic Par-4 mRNA and protein occurs in specific brain regions following TBI.
- The temporal expression pattern of Par-4 is consistent with its involvement in apoptosis and neuronal cell death after traumatic brain injury.
