Expression of basic fibroblast growth factor mRNA after transient focal ischemia: comparison with expression of
1Department of Neurosurgery, Nagoya City University, Medical School, Mizuho-ku, Nagoya, Japan.
Abstract:
We have reported that basic fibroblast growth factor (bFGF) prevents retrograde degeneration of thalamic neurons after middle cerebral artery (MCA) occlusion. To identify the protective mechanism of bFGF, we examined bFGF mRNA expression in a model of transient focal ischemia with in situ hybridization. Compared to c-fos, c-jun, and hsp 70 mRNA expression, upregulation of the bFGF mRNA expression was delayed until 6 h after reperfusion. By 12 h, bFGF mRNA was markedly induced in the peri-infarcted cortex, cingulate cortex, and peri-infarcted white matter. At 24 h and 2 days the induction of bFGF mRNA in these regions persisted, and disappeared by 5 day. The quantitative assessment of bFGF mRNA expression revealed that optical density ratios of the cingulate gyrus and the caudoputamen were significantly higher at 12 h, 24 h, and 2 d after reperfusion than those in sham controls. Microscopic observation indicated bFGF mRNA signals were present in several types of cortical cells, including neurons and nonneuronal cells. Since intrinsic bFGF, released from the damaged tissue, can influence the healing response through receptors upregulated by injury, it is reasonable that this pattern of bFGF mRNA expression parallels the bFGFR mRNA expression previously reported.
Insights
Basic fibroblast growth factor (bFGF) expression increases after stroke, particularly in brain regions surrounding the injury. This delayed upregulation suggests bFGF plays a role in the brain
Area of Science:
- Neuroscience
- Molecular Biology
- Ischemic Stroke Research
Background:
- Basic fibroblast growth factor (bFGF) is known to protect thalamic neurons from degeneration following middle cerebral artery (MCA) occlusion.
- The precise protective mechanism of bFGF in ischemic stroke remains to be fully elucidated.
Purpose of the Study:
- To investigate the temporal and spatial expression pattern of bFGF mRNA following transient focal cerebral ischemia.
- To understand the role of bFGF in the cellular response to ischemic injury.
Main Methods:
- Transient focal cerebral ischemia model in rodents.
- In situ hybridization to detect bFGF mRNA expression.
- Quantitative assessment of mRNA levels and microscopic cell type identification.
Main Results:
- bFGF mRNA upregulation was delayed, appearing 6 hours after reperfusion and peaking by 12 hours.
- Marked induction of bFGF mRNA was observed in peri-infarcted cortex, cingulate cortex, and white matter, persisting for up to 2 days.
- bFGF mRNA signals were detected in both neuronal and non-neuronal cells within the cortex.
Conclusions:
- The delayed and localized induction of bFGF mRNA suggests an endogenous protective response to ischemic injury.
- The expression pattern of bFGF mRNA parallels that of its receptor (bFGFR), indicating a potential autocrine or paracrine signaling pathway.
- Intrinsic bFGF released from damaged tissue may contribute to neuroprotection and tissue repair following stroke.
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