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Published on: September 11, 2017
Changes of bcl-x(L) and bax mRNA expression following traumatic brain injury in rats
Chun Luo1, Yicheng Lu, Jiyao Jiang
1Department of Neurosurgery, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China. luochun@sh163a.sta.net
Objective:
To investigate the changes of bcl-2 gene family and the molecular mechanism of neuronal apoptosis following traumatic brain injury (TBI) in rats.
Methods:
Male Sprague-Dawley (SD) rats were subjected to lateral fluid percussion brain injury (FPBI) of moderate severity. The bcl-x(L) and bax mRNA expression was detected by reverse transcription polymerase chain reaction (RT-PCR). In addition to morphological evidence of apoptosis, terminal deoxynucleotide transferase-mediated dUTP-biotin nick-end labeling (TUNEL) histochemistry was used to identify the DNA fragmentation in situ at both light and electron microscope levels, whereas characteristic internucleosomal DNA fragmentation of apoptosis was demonstrated by DNA gel electrophoresis.
Results:
The apoptotic response to trauma was regionally distinct and may be involved in both acute and delayed cell death. The bcl-x(L) mRNA expression of the impact site was significantly lower (67.42%+/-7.54%) than that of the ipsilateral hemisphere at 6 hours after injury (P<0.01). The decrease of bcl-x(L) mRNA expression preceded apoptosis at 24 hours after injury. The bax mRNA expression rose slowly, doubled at 3 days after injury and returned to the sham level slowly.
Conclusions:
Decreased expression of bcl-x(L) mRNA and increased expression of bax mRNA coincides with apoptosis following brain injury. The bcl-2 gene family is involved in neuronal apoptosis after TBI, and the changes of mRNA expression of the family members lead the neuronal cells to apoptosis.
Insights
Traumatic brain injury (TBI) in rats alters bcl-2 gene family expression, with decreased bcl-x(L) and increased bax mRNA preceding neuronal apoptosis. These changes in the bcl-2 gene family are key to understanding cell death after TBI.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Traumatic brain injury (TBI) is a significant cause of neuronal damage and death.
- The bcl-2 gene family plays a critical role in regulating apoptosis (programmed cell death).
Purpose of the Study:
- To investigate alterations in the bcl-2 gene family following traumatic brain injury (TBI).
- To elucidate the molecular mechanisms of neuronal apoptosis after TBI in a rat model.
Main Methods:
- Rats were subjected to lateral fluid percussion brain injury (FPBI).
- Reverse transcription polymerase chain reaction (RT-PCR) was used to measure bcl-x(L) and bax mRNA expression.
- Apoptosis was assessed using morphological analysis, TUNEL histochemistry, and DNA gel electrophoresis.
Main Results:
- Apoptosis following TBI was regionally distinct, contributing to both acute and delayed cell death.
- A significant decrease in bcl-x(L) mRNA expression was observed at the impact site, preceding observable apoptosis.
- bax mRNA expression increased over time, peaking at 3 days post-injury.
Conclusions:
- Decreased bcl-x(L) and increased bax mRNA expression correlate with neuronal apoptosis after TBI.
- The bcl-2 gene family is implicated in TBI-induced neuronal apoptosis.
- Changes in bcl-2 family mRNA expression appear to drive neuronal cell death following brain injury.
