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Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

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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Related Experiment Video

Updated: May 11, 2026

Investigating Angiogenesis on a Functional and Molecular Level by Leveraging the Scratch Wound Migration Assay and the Spheroid Sprouting Assay
09:16

Investigating Angiogenesis on a Functional and Molecular Level by Leveraging the Scratch Wound Migration Assay and the Spheroid Sprouting Assay

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SRF selectively controls tip cell invasive behavior in angiogenesis.

Claudio A Franco1, Jocelyne Blanc, Ara Parlakian

  • 1UPMC Univ Paris 06, UR 4, Aging, Stress and Inflammation, 75005 Paris, France. claudio.franco@cancer.org.uk

Development (Cambridge, England)
|May 16, 2013
PubMed
Summary
This summary is machine-generated.

Serum response factor (SRF) is vital for blood vessel growth and survival. Targeting SRF may inhibit tumor angiogenesis by affecting tip cell behavior.

Keywords:
ActinFilopodiaMouseMyosinSRFSprouting angiogenesis

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Last Updated: May 11, 2026

Investigating Angiogenesis on a Functional and Molecular Level by Leveraging the Scratch Wound Migration Assay and the Spheroid Sprouting Assay
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Area of Science:

  • Vascular biology
  • Molecular biology
  • Oncology

Background:

  • Angiogenic sprouting is crucial for development and disease.
  • Serum response factor (SRF) plays a role in embryonic vascular development.

Purpose of the Study:

  • To investigate the role of endothelial-specific SRF in postnatal and adult mice.
  • To determine SRF's requirement in developmental and pathological angiogenesis, including tumor growth.

Main Methods:

  • Inducible endothelial-specific deletion of Srf in mice.
  • Analysis of postnatal growth, survival, and angiogenesis.
  • Molecular analysis of SRF-dependent gene regulation.

Main Results:

  • Endothelial SRF is essential for postnatal survival and angiogenesis.
  • SRF is required for pathological angiogenesis and tumor growth.
  • SRF regulates endothelial filopodia formation and cell contractility.
  • SRF controls vascular endothelial growth factor A-induced MRTF nuclear accumulation and target gene expression (e.g., Myl9).

Conclusions:

  • SRF is critical for tip cell behavior during sprouting angiogenesis.
  • SRF is dispensable for vascular remodeling.
  • Targeting the SRF pathway may inhibit tumor growth by disrupting angiogenesis.