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Neuronal VEGF expression correlates with angiogenesis in postnatal developing rat brain.

O O Ogunshola1, W B Stewart, V Mihalcik

  • 1Department of Pediatrics, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06511, USA.

Brain Research. Developmental Brain Research
|January 29, 2000
PubMed
Summary
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Chronic hypoxia in developing rat brains increases blood vessel growth by altering vascular endothelial growth factor (VEGF) expression. This disruption in VEGF localization drives sustained angiogenesis.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Physiology

Background:

  • The developing brain's response to chronic hypoxia involves increased vascular permeability and angiogenesis.
  • Vascular endothelial growth factor (VEGF) is a potential mediator of this angiogenic response.

Purpose of the Study:

  • To investigate the localization of VEGF in the developing rat brain cortex.
  • To correlate VEGF expression patterns with vascularization changes under chronic hypoxia.

Main Methods:

  • Rats were reared under normoxic or hypoxic conditions (FiO(2) 9.5%) and analyzed at various postnatal days (P3-P33).
  • Techniques included immunohistochemistry, in situ hybridization (ISH), Western blot, and vessel density counting.
  • Platelet endothelial cell adhesion molecule 1 (PECAM-1) levels and microvascular parameters were assessed.

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Main Results:

  • Hypoxic exposure significantly increased PECAM-1 levels, microvascular lumen diameter, and vessel density compared to controls.
  • In normoxic conditions, VEGF expression shifted from neurons to glial cells during development.
  • Hypoxia maintained high neuronal VEGF expression and elevated glial cell expression, disrupting the normal temporal-spatial pattern.

Conclusions:

  • Chronic sublethal hypoxia disrupts the normal temporal-spatial expression of VEGF in the developing rat brain cortex.
  • This altered VEGF expression correlates with sustained hypoxia-driven angiogenesis and increased vascularization.