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Updated: Aug 9, 2026
Focal Cerebral Ischemia Model by Endovascular Suture Occlusion of the Middle Cerebral Artery in the Rat
Published on: February 6, 2011
p53-immunoreactive protein and p53 mRNA expression after transient middle cerebral artery occlusion in rats
1Department of Neurology, Henry Ford Hospital Health Science Center, Detroit, Mich.
Background And Purpose:
We investigated the temporal distribution of the p53-immunoreactive protein in conjunction with cellular damage and the expression of the p53 mRNA after focal cerebral ischemia in rats.
Methods:
Male Wistar rats (n = 66; controls, n = 7) were subjected to 2 hours of middle cerebral artery occlusion and were killed at various times of reperfusion (0.5 to 168 hours) for p53 immunohistochemistry and Northern blot analysis.
Results:
A cellular expression of mutant p53-immunoreactive protein was found localized to anatomic sites exhibiting severe neuronal damage. A maximal induction of mutant p53-immunoreactive protein was found at 12 hours after reperfusion and subsequently declined. No wild-type p53 protein expression was detected after ischemia. A time-dependent expression of p53 mRNA was observed in both hemispheres. The peak level of p53 mRNA occurred at 24 hours after reperfusion.
Conclusions:
Our data indicate that the expressions of p53-immunoreactive protein and p53 mRNA are upregulated after transient focal cerebral ischemic insult in rats. The concomitant appearance of p53 and cell damage in ischemic brain suggests that p53 expression may impact cell biological response to an ischemic insult.
Insights
p53 protein and mRNA expression increase after focal cerebral ischemia in rats, correlating with cell damage. This suggests p53 plays a role in the brain's response to ischemic injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Focal cerebral ischemia is a critical neurological event.
- The role of p53 in ischemic brain injury requires further elucidation.
Purpose of the Study:
- To investigate the temporal expression of p53 protein and mRNA following focal cerebral ischemia in a rat model.
- To correlate p53 expression patterns with cellular damage and neuronal injury.
Main Methods:
- Male Wistar rats underwent 2-hour middle cerebral artery occlusion.
- Samples were collected at various reperfusion times (0.5-168 hours).
- p53 immunohistochemistry and Northern blot analysis were performed.
Main Results:
- Mutant p53 protein expression localized to areas of severe neuronal damage.
- Maximal mutant p53 protein induction occurred at 12 hours post-reperfusion.
- p53 mRNA showed time-dependent expression in both hemispheres, peaking at 24 hours.
- No wild-type p53 protein was detected.
Conclusions:
- p53 protein and mRNA are upregulated following transient focal cerebral ischemia in rats.
- The co-occurrence of p53 expression and cell damage suggests a role for p53 in the cellular response to ischemic insult.
