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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

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Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
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Vascular endothelial growth factor-B expression in postischemic rat brain.

Lin Xie1, Xiaoou Mao1, Kunlin Jin2

  • 1Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA.

Vascular Cell
|April 23, 2013
PubMed
Summary

Stroke increases vascular endothelial growth factor-B (VEGF-B) expression in brain tissue. This protein is found in neurons and immune cells, suggesting a role in the brain's natural response to stroke injury.

Keywords:
IschemiaStrokeVascular endothelial growth factor-B (VEGF-B)

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cerebrovascular Research

Background:

  • Vascular endothelial growth factor-B (VEGF-B) is known to offer protection in experimental stroke models.
  • The precise impact of stroke on endogenous VEGF-B expression within the brain remains unclear.

Purpose of the Study:

  • To investigate the expression pattern of VEGF-B in the brain following ischemic stroke.
  • To determine the cellular localization of VEGF-B in the affected brain regions.

Main Methods:

  • Immunohistochemistry was employed to detect VEGF-B.
  • Expression was analyzed in the ischemic border zone of rat brains.
  • Samples were collected at intervals from 1 to 7 days post-middle cerebral artery occlusion.

Main Results:

  • VEGF-B immunoreactivity was significantly elevated in the ischemic border zone after middle cerebral artery occlusion.
  • VEGF-B was primarily localized to neurons and infiltrating macrophages/microglia.
  • No significant VEGF-B association was observed with astrocytes or endothelial cells in the studied area.

Conclusions:

  • The study demonstrates increased VEGF-B expression in response to cerebral ischemia.
  • Findings support a role for VEGF-B as part of the brain's intrinsic protective mechanisms against stroke.
  • VEGF-B's association with specific cell types highlights potential therapeutic targets.