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Related Experiment Videos

Experimental hypoxia and embryonic angiogenesis.

O Nanka1, P Valásek, M Dvoráková

  • 1Institute of Anatomy, Charles University First Faculty of Medicine, Prague, Czech Republic. ondrej.nanka@lfl.cuni.cz

Developmental Dynamics : an Official Publication of the American Association of Anatomists
|January 31, 2006
PubMed
Summary

Embryonic blood vessel formation relies on the hypoxia-inducible factor (HIF) and vascular endothelial growth factor (VEGF) pathway. Moderate hypoxia increases HIF and VEGF, leading to more blood vessels, showing oxygen levels influence development.

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Area of Science:

  • Developmental biology
  • Molecular biology
  • Physiology

Background:

  • Embryonic development involves complex processes, including angiogenesis (blood vessel formation).
  • Hypoxia (low oxygen) and Hypoxia-Inducible Factors (HIFs) are known regulators of angiogenesis in various contexts.
  • The precise role of oxygen tension and HIFs in normal embryonic vascular development requires further elucidation.

Purpose of the Study:

  • To investigate the role of hypoxia and HIF factors in embryonic angiogenesis.
  • To correlate the degree of hypoxia with HIF and VEGF expression and blood vessel formation during quail embryogenesis.

Main Methods:

  • Quail embryos were cultured under normoxic and hypoxic conditions (16% O2).
  • Tissue hypoxia was detected using pimonidazole hydrochloride and Hypoxyprobe-1 antibody.

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  • Expression of VEGF and HIF factors (HIF-1alpha, HIF-1beta, HIF-2alpha) was analyzed using in situ hybridization and Western blot.
  • Endothelial cells were identified using QH-1 antibody.

    • Main Results:

    • Hypoxic regions were identified in both normoxic and hypoxic embryos, primarily in the brain, neural tube, and mesonephros.
    • HIF-1alpha and HIF-1beta expression patterns generally followed hypoxic regions; HIF-2alpha was mainly in endothelial cells.
    • Vascular Endothelial Growth Factor (VEGF) expression was detected in hypoxic areas, particularly the mesonephros, and growing capillaries were directed towards VEGF-positive areas.
    • Increased hypoxia led to larger, more intensely stained hypoxic regions, with proportional increases in HIF-1 and VEGF expression and enhanced angiogenesis.

    Conclusions:

    • Normal embryonic vascular development utilizes the HIF-VEGF regulatory cascade.
    • Embryonic angiogenesis is responsive to environmental oxygen tension, indicating it is not solely genetically controlled.
    • Experimentally increasing hypoxia upregulates HIF and VEGF, subsequently increasing blood vessel density.