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Updated: Jun 21, 2025

In Vitro Model of Coronary Angiogenesis
Published on: March 10, 2020
Early growth response factor 3 may regulate coronary atherosclerosis through the NF-κB signaling pathway and VEGF
Zumureti Abudukeyimu1, Junyi Luo2, Fang Liu1
1Department of General Practice, the Fifth Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, 830001, China.
Insights
Early Growth Response 3 (Egr3) gene expression is elevated in coronary artery disease (CAD) and promotes atherosclerosis by increasing inflammatory factors and lipid accumulation. Inhibiting Egr3 reduces these effects, suggesting Egr3 as a potential therapeutic target for CAD.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Inflammation Research
Background:
- Coronary artery disease (CAD) is a complex condition involving inflammation and endothelial dysfunction.
- The role of specific gene expression, such as Early Growth Response 3 (Egr3), in CAD pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the expression of Egr3, inflammatory cytokines (IL-1β, IL-6), vascular endothelial growth factor (VEGF), and NF-κB in CAD patients.
- To explore the relationship between Egr3 gene expression and these molecules in the context of CAD.
Main Methods:
- Recruited 132 CAD patients and 63 healthy controls.
- Measured gene and protein expression using RT-qPCR, ELISA, and Western blotting.
- Utilized an in vitro atherosclerosis model with human coronary artery endothelial cells (HCAECs) treated with ox-LDL.
Main Results:
- Egr3 and IL-6 serum levels were higher in severe CAD patients compared to mild stenosis and controls.
- Egr3 expression positively correlated with IL-6, IL-1β, and Gensini score.
- Inhibition of Egr3 in vitro reduced inflammatory markers, lipid droplet formation, and lumen formation capacity.
Conclusions:
- Egr3 gene expression plays a significant role in promoting atherosclerosis development.
- Egr3 may induce inflammatory factors and affect lipid and lumen formation, contributing to CAD pathogenesis.
- Egr3 represents a potential therapeutic target for managing atherosclerosis.
Aim:
The present study was conducted to measure the expression of early growth response factor 3 (Egr3), inflammatory cytokines (IL-1β, IL-6), vascular endothelial growth factor (VEGF) and NF-κB in patients with coronary artery disease (CAD) to investigate the relationships of these molecules and Egr3 gene expression.
Methods:
We recruited 132 CAD patients and 63 healthy individuals. The expression levels of Egr3, VEGF, p50 and p65 were measured by reverse transcription quantitative polymerase chain reaction and the levels of Egr3, IL-1β and IL-6 in patients serum and in human coronary artery endothelial cells (HCAECs) were measured by enzyme-linked immunosorbent assay (ELISAs) in CAD patients. HCAECs were treated with ox-LDL to establish an in vitro atherosclerosis model. An oil red O staining assay was used to assess the lipid droplet formation. A colloidal external lumen formed by Matrigel was used to test the migration of HCAECs. The expression of Egr3, VEGF and NF-κB was determined by Western blotting.
Results:
The levels of serum Egr3 and IL-6 in the severe stenosis group were greater than those in the mild stenosis group and controls (p < 0.05). The level of serum IL-1β in the severe stenosis group was greater than that in the control group (p < 0.05). Moreover, Egr3 expression was positively associated with IL-6 levels (r = 0.55, p < 0.001), IL-1β levels (r = 0.21, p = 0.004) and the Gensini score (r = 0.20, p = 0.02). We also found that Egr3 expression was significantly greater in CAD patients than that in controls. And its expression was highest in the mild patients. The expression of VEGF, P50 and P65 was also greater in CAD patients. In the in vitro experiment, we found that the inhibition of Egr3 expression significantly reduced the expression levels of p50, p65, IL-6 and CRP. Moreover, the inhibition of Egr3 expression significantly reduced the lipid droplet formation and decreased capability of lumen formation.
Conclusions:
In the pathogenesis of atherosclerosis, Egr3 gene expression may induce the expression of inflammatory factors and lipid droplet formation and lumen formation, which could promote the atherosclerosis development.
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