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Related Concept Videos

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...
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...
Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the exudate's...
Overview of Regeneration and Repair01:19

Overview of Regeneration and Repair

Regeneration and repair processes are critical in healing damages caused by injury, disease, and aging. In regeneration, the damaged tissue is entirely replaced with new growth that restores the original architecture and function. In contrast, tissue repair usually results in a fixed tissue architecture involving scar formation. Scars generally do not reestablish tissue function and may also exhibit structural abnormalities at the injury site.
Regeneration
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Phases of Wound Repair01:28

Phases of Wound Repair

Following injury, the integrity of the injured tissues must be reestablished. For example, in skin tissue, wound repair involves coordination among resident skin cells, blood mononuclear cells, extracellular matrix, growth factors, and cytokines to complete the healing cascade.
Formation of Blood Clot
In case of deep injuries, trauma to blood vessels results in blood loss. In the meantime, phospholipids released from the ruptured endothelial cellular membrane are converted into arachidonic...
Healing I: Introduction01:11

Healing I: Introduction

Healing is the physiological process by which the body restores the integrity and function of damaged tissues following injury. It involves a coordinated interplay of cellular proliferation, extracellular matrix remodeling, and growth factor signaling. The extent and nature of the tissue damage determine whether healing occurs by resolution, regeneration, or replacement.ResolutionResolution represents the most complete form of healing, occurring when the injury is minimal and tissue...

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Related Experiment Video

Updated: Jul 8, 2026

A Full Skin Defect Model to Evaluate Vascularization of Biomaterials In Vivo
07:56

A Full Skin Defect Model to Evaluate Vascularization of Biomaterials In Vivo

Published on: August 28, 2014

Angiogenesis in wound healing.

M G Tonnesen1, X Feng, R A Clark

  • 1Department of Dermatology, State University of New York at Stony Brook, 11794-8165, USA.

The Journal of Investigative Dermatology. Symposium Proceedings
|January 9, 2001
PubMed
Summary
This summary is machine-generated.

During wound healing, the integrin receptor alpha(v)beta3 is crucial for new blood vessel formation (angiogenesis). Its expression on endothelial cells is regulated by the wound

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

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Last Updated: Jul 8, 2026

A Full Skin Defect Model to Evaluate Vascularization of Biomaterials In Vivo
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Published on: August 28, 2014

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Murine Excisional Wound Healing Model and Histological Morphometric Wound Analysis

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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

Published on: May 31, 2024

Area of Science:

  • Biomedical Engineering
  • Cell Biology
  • Wound Healing Research

Background:

  • Wound healing involves complex interactions between endothelial cells, angiogenic factors, and the extracellular matrix (ECM).
  • Initially, capillary sprouts form a microvascular network in a fibrin/fibronectin-rich clot, which later diminishes as collagen accumulates.
  • Endothelial cell ECM receptors, like alpha(v)beta3 integrin, play a critical role in blood vessel morphogenesis during repair.

Purpose of the Study:

  • To investigate the role of the alpha(v)beta3 integrin receptor in wound angiogenesis.
  • To understand how the wound ECM environment regulates integrin expression and endothelial cell behavior.
  • To explore the potential for targeting these mechanisms in treating chronic wounds.

Main Methods:

  • Examined alpha(v)beta3 integrin expression on angiogenic capillary sprouts in wound environments.
  • Utilized functional inhibitors of alpha(v)beta3 to assess their impact on granulation tissue formation.
  • Investigated alpha(v)beta3 mRNA levels in human dermal microvascular endothelial cells cultured on different ECM components (fibronectin, fibrin, collagen).
  • Employed an in vitro model of sprout angiogenesis using three-dimensional fibrin and collagen gels.

Main Results:

  • Alpha(v)beta3 integrin is expressed on capillary sprouts invading the wound clot and is essential for wound angiogenesis.
  • Inhibiting alpha(v)beta3 transiently hinders granulation tissue formation.
  • Wound ECM modulates alpha(v)beta3 expression; higher mRNA levels were observed on fibronectin and fibrin compared to collagen.
  • Three-dimensional fibrin gel, mimicking early wound clot, supported angiogenesis in vitro, unlike collagen gel.

Conclusions:

  • The alpha(v)beta3 integrin receptor is vital for wound angiogenesis, with its expression influenced by the ECM.
  • The dynamic ECM environment, particularly fibrin, supports early angiogenesis, while collagen dominates later scar tissue formation.
  • Understanding ECM-integrin-angiogenic factor interactions offers therapeutic avenues for chronic wound management.