Expression of basic fibroblast growth factor receptor messenger RNA in the periinfarcted brain tissue

T Sakaguchi1, K Yamada, A Wanaka

  • 1Department of Neurosurgery, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan.

Insights

Basic fibroblast growth factor receptor (bFGFR) messenger ribonucleic acid (mRNA) expression increased in brain areas surrounding focal ischemia in rats. This upregulation in periinfarcted tissue suggests bFGF may protect neurons from ischemic injury.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Ischemic Stroke Research

Background:

  • Focal ischemia, such as middle cerebral artery (MCA) occlusion, causes significant neuronal damage.
  • Basic fibroblast growth factor (bFGF) is a potent neurotrophic factor with potential therapeutic roles in stroke.
  • Understanding the expression patterns of bFGF receptors is crucial for elucidating its protective mechanisms.

Purpose of the Study:

  • To investigate the spatiotemporal expression of basic fibroblast growth factor receptor (bFGFR) messenger ribonucleic acid (mRNA) following focal cerebral ischemia.
  • To determine if bFGFR mRNA upregulation occurs in the periinfarcted region after middle cerebral artery (MCA) occlusion in a rat model.
  • To explore the cellular localization of bFGFR mRNA in ischemic brain tissue.

Main Methods:

  • Establishment of a rat model of middle cerebral artery (MCA) occlusion to induce focal ischemia.
  • In situ hybridization autoradiography using 35S-labeled antisense RNA probes to detect bFGFR mRNA expression.
  • Analysis of brain sections at 1, 3, 7, and 14 days post-MCA occlusion, comparing with sham controls.

Main Results:

  • Upregulation of bFGFR mRNA was observed in the periinfarcted area of the ipsilateral hemisphere within 1 to 14 days after MCA occlusion.
  • Expression levels were particularly high at 1 and 3 days post-ischemia, with no detectable expression in the contralateral hemisphere.
  • Microautoradiography revealed bFGFR mRNA signals in both neurons and non-neural cells within the periinfarcted zone.

Conclusions:

  • The observed upregulation of bFGFR mRNA in periinfarcted brain tissue suggests a role for bFGF signaling in the ischemic cascade.
  • The presence of bFGFR mRNA in both neuronal and non-neuronal cells indicates a broad cellular response to ischemia.
  • These findings support the hypothesis that receptor-mediated actions of bFGF may contribute to the preservation of neurons injured by focal ischemia.

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