Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

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...
Development of Blood Vessels01:07

Development of Blood Vessels

The development of the vascular system in a fetus is a complex and intricate process that begins as early as 15 to 16 days post-conception. This process starts outside the embryo, specifically in the mesoderm of the yolk sac, chorion, and connecting stalk. Approximately two days later, the formation of blood vessels occurs within the embryo itself.
The initial formation of this system is facilitated by the small amount of yolk present in the ovum and yolk sac. Blood vessels originate from...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

RelB drives integrin-mediated stress tolerance and relapse in high-grade serous ovarian cancer.

Cell reports·2026
Same author

Global trends (1990-2021) and trojections to 2050 in alcohol-attributable epilepsy burden among adults over 40 years old.

BMC public health·2025
Same author

A study on identifying the phenotypic saturation thresholds of broomcorn millet based on functional limits and growth models.

PloS one·2025
Same author

Macrophage-Engaging IgG4 Antibody Triggers Cytotoxicity against Integrin αvβ3+ Cancers.

Molecular cancer therapeutics·2025
Same author

Efficacy and safety of Shouhui Tongbian Capsules, a traditional Chinese medicine, combined with 2L polyethylene glycol for bowel preparation before colonoscopy: a multicenter, randomized, single-blind, parallel-controlled clinical trial.

Therapeutic advances in gastroenterology·2025
Same author

A STAT3/integrin axis accelerates pancreatic cancer initiation and progression.

Cell reports·2025

Related Experiment Video

Updated: Jul 19, 2026

In Vitro Model of Coronary Angiogenesis
08:03

In Vitro Model of Coronary Angiogenesis

Published on: March 10, 2020

Cooperation between VEGF and beta3 integrin during cardiac vascular development.

Sara M Weis1, Jeffrey N Lindquist, Leo A Barnes

  • 1Moores UCSD Cancer Center, University of California, San Diego, CA 92093-0803, USA.

Blood
|October 26, 2006
PubMed
Summary

Beta3 integrin is crucial for coronary vascular development in male mice. Its absence leads to immature blood vessels, a condition linked to enhanced vascular endothelial growth factor (VEGF) signaling.

More Related Videos

A Method for Labeling Vasculature in Embryonic Mice
09:58

A Method for Labeling Vasculature in Embryonic Mice

Published on: October 7, 2011

En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos
08:57

En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos

Published on: July 27, 2022

Related Experiment Videos

Last Updated: Jul 19, 2026

In Vitro Model of Coronary Angiogenesis
08:03

In Vitro Model of Coronary Angiogenesis

Published on: March 10, 2020

A Method for Labeling Vasculature in Embryonic Mice
09:58

A Method for Labeling Vasculature in Embryonic Mice

Published on: October 7, 2011

En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos
08:57

En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos

Published on: July 27, 2022

Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Angiogenesis Research

Background:

  • Neovascularization in the developing heart relies on vascular endothelial growth factor (VEGF).
  • Beta3 integrin expression decreases as coronary vessels mature post-birth.
  • Integrins are key regulators of cell adhesion and signaling in vascular development.

Purpose of the Study:

  • To investigate the role of beta3 integrin in coronary vascular development and maturation.
  • To determine the impact of beta3 integrin deficiency on the response to VEGF signaling.
  • To elucidate the sex-specific effects of beta3 integrin absence on cardiac vasculature.

Main Methods:

  • Analysis of coronary vascular morphology in beta3 integrin-null mice (male and female).
  • Assessment of vascular endothelial growth factor (VEGF) and Flk-1 signaling pathways.
  • Pharmacological inhibition of VEGF and Flk-1 in beta3-null mice.
  • Induction of angiogenic phenotypes via VEGF injection in wild-type mice.

Main Results:

  • Male beta3-null mice exhibit immature coronary capillaries with irregular endothelial structure.
  • The observed vascular phenotype in beta3-null mice is exacerbated by enhanced VEGF signaling.
  • Inhibition of VEGF or Flk-1 normalizes the vascular defects in beta3-null mice.
  • Female beta3-null mice do not display the same vascular phenotype.
  • VEGF administration induces an angiogenic phenotype in wild-type adult mouse hearts.

Conclusions:

  • Beta3 integrin plays a critical role in coronary vascular development and maturation.
  • The absence of beta3 integrin leads to abnormal vascular remodeling, particularly in males.
  • Beta3 integrin influences the heart's vascular response to VEGF signaling.