Related Experiment Video
Updated: Jul 19, 2026
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
Angiogenesis and vasculogenesis in systemic sclerosis
J H W Distler1, S Gay, O Distler
1Department of Internal Medicine III, University of Erlangen-Nuremberg, Germany.
Rheumatology (Oxford, England)
|September 22, 2006
Summary
Systemic sclerosis (SSc) involves vascular damage and impaired blood vessel formation. Paradoxical vascular endothelial growth factor (VEGF) overexpression in SSc may contribute to abnormal vessel development, despite its potential to heal ulcers.
Area of Science:
- Rheumatology
- Vascular Biology
- Pathogenesis of Systemic Sclerosis
Background:
- Systemic sclerosis (SSc) is characterized by vascular changes, inflammation, and extracellular matrix accumulation.
- Endothelial cell apoptosis and damage markers are elevated in SSc patients.
- Despite insufficient angiogenesis, vascular endothelial growth factor (VEGF) is overexpressed in SSc.
Purpose of the Study:
- To investigate the role of vascular endothelial growth factor (VEGF) in the pathogenesis of systemic sclerosis (SSc).
- To explore the paradoxical effects of VEGF overexpression on vascular development in SSc.
- To examine the contribution of impaired vasculogenesis and endothelial progenitor cells to SSc vascular defects.
Main Methods:
- Analysis of endothelial cell apoptosis markers in SSc patients.
- Assessment of vascular endothelial growth factor (VEGF) levels and its correlation with angiogenesis.
- Evaluation of endothelial progenitor cell number and function in SSc.
Main Results:
- Elevated markers of endothelial cell damage and apoptosis in SSc.
- Overexpression of vascular endothelial growth factor (VEGF) in SSc patients.
- Paradoxical effects of prolonged VEGF overexpression leading to irregular vessel formation.
- Impaired vasculogenesis due to reduced and functionally deficient endothelial progenitor cells in SSc.
Conclusions:
- Vascular changes, including impaired angiogenesis and vasculogenesis, are central to SSc pathogenesis.
- Overexpressed VEGF in SSc may paradoxically promote abnormal vascular remodeling rather than effective angiogenesis.
- Defects in endothelial progenitor cells further contribute to the vascular complications observed in SSc.
Related Concept Videos
01:10Mechanism 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...
01:24Regulation 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...
01:20Overview of the Vascular System
The vascular system comprises an extensive network of arteries, capillaries, and veins. The vascular system can be broadly divided into the blood and lymphatic systems. Typically, blood vessels can be categorized into three histological regions: tunica intima, tunica media, and tunica adventitia. The tunica intima consists of a single layer of endothelial cells attached to the basal lamina. Underlying the basal lamina is a connective tissue layer and an elastic lamina that gives stability and...