{"title":"早期生长应答因子 3 通过 NF-κB 信号通路和血管内皮生长因子的表达调控冠状动脉粥样硬化。","authors":"","doi":"10.1016/j.amjms.2024.07.003","DOIUrl":null,"url":null,"abstract":"<div><h3>Aim</h3><div>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.</div></div><div><h3>Methods</h3><div>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.</div></div><div><h3>Results</h3><div>The levels of serum Egr3 and IL-6 in the severe stenosis group were greater than those in the mild stenosis group and controls (<em>p</em> < 0.05). The level of serum IL-1β in the severe stenosis group was greater than that in the control group (<em>p</em> < 0.05). Moreover, Egr3 expression was positively associated with IL-6 levels (<em>r</em> = 0.55, <em>p</em> < 0.001), IL-1β levels (<em>r</em> = 0.21, <em>p</em> = 0.004) and the Gensini score (<em>r</em> = 0.20, <em>p</em> = 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.</div></div><div><h3>Conclusions</h3><div>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.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"368 5","pages":"Pages 476-484"},"PeriodicalIF":2.3000,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Early growth response factor 3 may regulate coronary atherosclerosis through the NF-κB signaling pathway and VEGF expression\",\"authors\":\"\",\"doi\":\"10.1016/j.amjms.2024.07.003\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Aim</h3><div>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.</div></div><div><h3>Methods</h3><div>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.</div></div><div><h3>Results</h3><div>The levels of serum Egr3 and IL-6 in the severe stenosis group were greater than those in the mild stenosis group and controls (<em>p</em> < 0.05). The level of serum IL-1β in the severe stenosis group was greater than that in the control group (<em>p</em> < 0.05). Moreover, Egr3 expression was positively associated with IL-6 levels (<em>r</em> = 0.55, <em>p</em> < 0.001), IL-1β levels (<em>r</em> = 0.21, <em>p</em> = 0.004) and the Gensini score (<em>r</em> = 0.20, <em>p</em> = 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.</div></div><div><h3>Conclusions</h3><div>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.</div></div>\",\"PeriodicalId\":55526,\"journal\":{\"name\":\"American Journal of the Medical Sciences\",\"volume\":\"368 5\",\"pages\":\"Pages 476-484\"},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2024-07-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American Journal of the Medical Sciences\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0002962924013387\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of the Medical Sciences","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0002962924013387","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
Early growth response factor 3 may regulate coronary atherosclerosis through the NF-κB signaling pathway and VEGF expression
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.
期刊介绍:
The American Journal of The Medical Sciences (AJMS), founded in 1820, is the 2nd oldest medical journal in the United States. The AJMS is the official journal of the Southern Society for Clinical Investigation (SSCI). The SSCI is dedicated to the advancement of medical research and the exchange of knowledge, information and ideas. Its members are committed to mentoring future generations of medical investigators and promoting careers in academic medicine. The AJMS publishes, on a monthly basis, peer-reviewed articles in the field of internal medicine and its subspecialties, which include:
Original clinical and basic science investigations
Review articles
Online Images in the Medical Sciences
Special Features Include:
Patient-Centered Focused Reviews
History of Medicine
The Science of Medical Education.