scholarly journals Coronary Artery Disease Increases the Long Noncoding RNA PUNISHER in Small Extracellular Vesicles and Regulates Endothelial Cell Function via Vesicular Shuttling

2021 ◽  
Author(s):  
Mohammed Rabiul Hosen ◽  
Qian Li ◽  
Yangyang Liu ◽  
Andreas Zietzer ◽  
Katharina Maus ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Cell ◽  
Coronary Artery ◽  
Extracellular Vesicles ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cell Function ◽  
Endothelial Cell Function ◽  
Artery Disease

Changes in blood dendritic cell counts in relation to type of coronary artery disease and brachial endothelial cell function

2010 ◽  
Vol 21 (2) ◽  
pp. 87-96 ◽  
Author(s):  
Emily A. Van Vré ◽  
Ilse Van Brussel ◽  
Ken Op de Beeck ◽  
Vicky Y. Hoymans ◽  
Christiaan J. Vrints ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Cell ◽  
Coronary Artery ◽  
Dendritic Cell ◽  
Cell Function ◽  
Endothelial Cell Function ◽  
Cell Counts ◽  
Artery Disease ◽  
Blood Dendritic Cell

Down-regulated RGS5 by genetic variants impairs endothelial cell function and contributes to coronary artery disease

2019 ◽  
Author(s):  
Yang Li ◽  
Han Yan ◽  
Jian Guo ◽  
Yingchun Han ◽  
Cuifang Zhang ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Cell ◽  
Coronary Artery ◽  
Genetic Variants ◽  
Cell Function ◽  
Association Studies ◽  
Genome Wide Association Studies ◽  
Endothelial Cell Function ◽  
Genome Wide ◽  
Artery Disease

Abstract Aims Genetic contribution to coronary artery disease (CAD) remains largely unillustrated. Although transcriptomic profiles have identified dozens of genes that are differentially expressed in normal and atherosclerotic vessels, whether those genes are genetically associated with CAD remains to be determined. Here, we combined genetic association studies, transcriptome profiles and in vitro and in vivo functional experiments to identify novel susceptibility genes for CAD. Methods and results Through an integrative analysis of transcriptome profiles with genome-wide association studies for CAD, we obtained 18 candidate genes and selected one representative single nucleotide polymorphism (SNP) for each gene for multi-centred validations. We identified an intragenic SNP, rs1056515 in RGS5 gene (odds ratio = 1.17, 95% confidence interval =1.10–1.24, P = 3.72 × 10−8) associated with CAD at genome-wide significance. Rare genetic variants in linkage disequilibrium with rs1056515 were identified in CAD patients leading to a decreased expression of RGS5. The decreased expression was also observed in atherosclerotic vessels and endothelial cells treated by various cardiovascular risk factors. Through siRNA knockdown and adenoviral overexpression, we further showed that RGS5 regulated endothelial inflammation, vascular remodelling, as well as canonical NF-κB signalling activation. Moreover, CXCL12, a specific downstream target of the non-canonical NF-κB pathway, was strongly affected by RGS5. However, the p100 processing, a well-documented marker for non-canonical NF-κB pathway activation, was not altered, suggesting an existence of a novel mechanism by which RGS5 regulates CXCL12. Conclusions We identified RGS5 as a novel susceptibility gene for CAD and showed that the decreased expression of RGS5 impaired endothelial cell function and functionally contributed to atherosclerosis through a variety of molecular mechanisms. How RGS5 regulates the expression of CXCL12 needs further studies.

scholarly journals 537Microparticles and exosomes differentially impact on endothelial cell function in coronary artery disease

2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S98.2-S98
Author(s):  
N Kraenkel ◽  
S Briand ◽  
E Straessler ◽  
M Uhlemann ◽  
V Adams ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Cell ◽  
Coronary Artery ◽  
Cell Function ◽  
Endothelial Cell Function ◽  
Artery Disease

scholarly journals Relationship between Long Noncoding RNA H19 Polymorphisms and Risk of Coronary Artery Disease in a Chinese Population: A Case-Control Study

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Wei-na Hu ◽  
Han-xi Ding ◽  
Qian Xu ◽  
Xue-ying Zhang ◽  
Da-tong Yang ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Long Noncoding Rna ◽  
Chinese Population ◽  
Noncoding Rna ◽  
Case Control Study ◽  
Case Control ◽  
Major Health Problem ◽  
Artery Disease ◽  
Control Study

Background/Aim. Coronary artery disease (CAD) is a major health problem that has high morbidity and mortality around the world. In recent years, long noncoding RNA H19 has been reported to affect the proliferation and apoptosis of vascular cells, which directly or indirectly results in atherosclerosis. We performed a case-control study to explore the relationship between H19 gene polymorphisms (rs2735971, rs2839698, and rs3024270) and the risk of CAD. Methods. We collected 732 samples from Liaoning Province, China, and three polymorphisms in long noncoding RNA H19 were genotyped using the KASP platform. Results. Our data showed that H19 rs2735971 and rs3024270 variant genotypes were associated with a decreased risk of CAD (rs2735971, P=0.003, odds ratio OR=0.6195, 95% confidence interval=0.44−0.84; rs3024270, P=0.030, OR=0.65, 95% confidence interval=0.44−0.96). No significant association with the risk of CAD was found for H19 rs2839698 polymorphism (P>0.05). In haplotype analysis, H19 polymorphisms of rs2735971-rs2839698-rs3024270 A-C-C haplotype reduced the risk of CAD by 0.61-fold (P=0.004, OR=0.61, 95% confidence interval=0.43–0.86). In addition, we found that rs2839698 interacted with smoking (Pinteraction=0.027), and according to multifactor dimensionality reduction analysis, the three-factor model including H19 rs2839698-smoking-drinking was the best model for the risk of CAD (testing balanced accuracy=0.6979). Conclusion. Our study demonstrated that some genotypes of H19 rs2735971 and rs3024270 polymorphisms, as well as rs2735971-rs2839698-rs3024270 A-C-C haplotype, were associated with the risk of CAD in a Chinese population, and these genotypes have the potential to be biomarkers for predicting CAD risk. We also found that rs2735971-rs2839698-rs3024270 A-C-C may have a significantly lower risk of CAD. The recessive genetic model of rs3024270 could predict the severity of CAD.

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