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Related Concept Videos

Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

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Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
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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...
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Prostate angiogenesis in development and inflammation.

Letitia Wong1, Jerry Gipp, Jason Carr

  • 1Department of Urology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin; Molecular and Environmental Toxicology Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.

The Prostate
|December 3, 2013
PubMed
Summary
This summary is machine-generated.

Prostate inflammation increases blood vessel growth and endothelial cell proliferation. However, it surprisingly reduces pro-angiogenic factors, suggesting inflammation uses different mechanisms than normal prostate development.

Keywords:
developmentinflammationprostatevasculature

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Area of Science:

  • Urology
  • Vascular Biology
  • Inflammation Research

Background:

  • Prostatic inflammation is linked to benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS).
  • Understanding prostate vascular development and response to inflammation is crucial.

Purpose of the Study:

  • Characterize normal mouse prostate vascular anatomy and development.
  • Investigate the impact of bacterial-induced inflammation on prostate vasculature.

Main Methods:

  • India ink perfusion for vascular visualization.
  • Immunostaining for vascular development.
  • Transurethral bacterial instillation to induce inflammation.
  • RT-PCR and BrdU labeling for gene expression and cell proliferation.

Main Results:

  • Detailed description of the prostatic arterial supply.
  • Normal vascular development involves endothelial proliferation and pro-angiogenic factors.
  • Bacterial prostatitis increased vascular density and endothelial proliferation but decreased pro-angiogenic factor expression.

Conclusions:

  • Prostate inflammation triggers endothelial proliferation and increased vascularity.
  • The molecular regulation of vascular response to inflammation differs from normal development.
  • Inflammation may involve distinct regulatory mechanisms for endothelial cells.