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Monocyte chemoattractant protein-1 messenger RNA expression in rat ischemic cortex
1Department of Cardiovascular Pharmacology, SmithKline Beecham Pharmaceuticals, King of Prussia, PA 19406, USA.
Stroke
|April 1, 1995
Summary
Monocyte chemoattractant protein-1 (MCP-1) messenger RNA (mRNA) is significantly increased in ischemic brain tissue after middle cerebral artery occlusion (MCAO). This early MCP-1 mRNA expression suggests its role in monocyte infiltration and potential contribution to stroke injury.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Focal cerebral ischemia, induced by middle cerebral artery occlusion (MCAO), leads to increased cytokine/chemokine expression.
- Monocyte chemoattractant protein-1 (MCP-1) is a specific chemoattractant for monocytes, crucial in inflammatory responses.
Purpose of the Study:
- To investigate the expression of MCP-1 messenger RNA (mRNA) in ischemic brain tissue following MCAO.
- To determine if MCP-1 mRNA is upregulated in the early stages of focal cerebral ischemia.
Main Methods:
- Reverse transcription and polymerase chain reaction (RT-PCR) were used to initially detect MCP-1 mRNA.
- Northern blot analysis quantified MCP-1 mRNA expression over time in ischemic and non-ischemic brain regions after permanent and temporary MCAO with reperfusion.
Main Results:
- MCP-1 mRNA expression was significantly elevated in the ischemic cortex post-MCAO, with minimal expression in sham or non-ischemic tissue.
- Expression peaked between 12 hours and 2 days after permanent MCAO (22.7-fold increase) and was elevated for up to 5 days.
- Following MCAO with reperfusion, MCP-1 mRNA increased earlier (3 hours) and was higher in hypertensive rats compared to normotensive rats.
Conclusions:
- Induced MCP-1 mRNA expression occurs early after focal ischemia, indicating its potential role as a local chemoattractant.
- MCP-1 likely contributes to monocyte infiltration into ischemic brain tissue, potentially exacerbating stroke-related injury.
- Further research is needed to identify MCP-1's specific cellular localization within the ischemic brain.