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Regional expression of Bcl-2 mRNA and mitochondrial cytochrome c release after experimental brain injury in the rat
G X Dong1, D K Singh, P Dendle
1Division of Neurosurgery, Department of Surgery and Sanders Brown Center on Aging, University of Kentucky Chandler Medical Center, Lexington, KY 40536-0084, USA.
Abstract:
Regional levels of anti-apoptotic Bcl-2 mRNA and the cytosolic cytochrome c protein were measured after lateral fluid percussion (FP) brain injury in rats. Levels of Bcl-2 mRNA were significantly decreased in the injured left cortex (IC) and ipsilateral hippocampus (IH), but not in the contralateral right cortex (CC) and hippocampus (CH) after brain injury. Levels of Bcl-2 mRNA were significantly decreased as early as 2 h and stayed decreased as long as 48 h in the IC and IH after injury. Levels of the cytosolic cytochrome c protein were significantly increased in the IC and IH, but not in the CC and CH after brain injury. Levels of cytosolic cytochrome c were significantly increased in the IC at 30 min, 48 and 72 h, and in the IH at 2 h and as long as 72 h after injury. The increase of cytosolic cytochrome c suggests that the mitochondrial release of cytochrome is increased in the IC and IH after lateral FP brain injury. These data show that the reduction of anti-apoptotic Bcl-2 and increases of mitochondrial release of cytochrome c protein occur only in the IC and IH, regions which have been observed to undergo apoptosis and neuronal cell loss after lateral FP brain injury. Therefore, it is likely that the reduction of Bcl-2 and the increased cytochrome c protein in the cytosol contribute to the observed apoptosis and neuronal cell death in the IC and IH after lateral FP brain injury in rats.
Insights
Brain injury in rats reduces anti-apoptotic Bcl-2 mRNA and increases cytosolic cytochrome c, suggesting these changes contribute to neuronal cell death in injured brain regions.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Traumatic brain injury (TBI) can lead to neuronal cell loss.
- The Bcl-2 family of proteins plays a critical role in regulating apoptosis.
- Cytochrome c release from mitochondria is a key event in the apoptotic pathway.
Purpose of the Study:
- To investigate the regional changes in anti-apoptotic Bcl-2 mRNA and cytosolic cytochrome c protein following lateral fluid percussion (FP) brain injury in rats.
- To determine the correlation between these molecular changes and observed neuronal apoptosis and cell loss.
Main Methods:
- Measurement of Bcl-2 mRNA levels using quantitative methods.
- Assessment of cytosolic cytochrome c protein levels via biochemical assays.
- Induction of brain injury using the lateral fluid percussion (FP) model in a rat.
- Analysis of molecular changes in specific brain regions (injured cortex and hippocampus).
Main Results:
- Bcl-2 mRNA levels significantly decreased in the injured cortex and ipsilateral hippocampus, but not in contralateral regions.
- Cytosolic cytochrome c protein levels significantly increased in the injured cortex and ipsilateral hippocampus.
- These molecular changes were observed as early as 30 minutes to 2 hours post-injury and persisted for up to 72 hours.
Conclusions:
- The reduction in anti-apoptotic Bcl-2 and the increase in mitochondrial release of cytochrome c are localized to brain regions experiencing apoptosis and neuronal cell loss after FP brain injury.
- These molecular alterations likely contribute to the observed apoptosis and neuronal cell death in the injured brain.