scholarly journals The abnormal regulation of spliceosome may be a key factor for coronary heart disease: a simple bioinformatics analysis

2020 ◽  
Author(s):  
Zhaoshui Li ◽  
Wei Sheng ◽  
Yifan Chi
Keyword(s):  
Gene Expression ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Gene Expression Omnibus ◽  
Network Control ◽  
Biological Database ◽  
Bioinformatics Analyses ◽  
Chain Reactions ◽  
Go Annotation ◽  
Key Factor

Abstract Background: Cardiovascular Diseases (CVDs) has become a major disease threatening human health. As the main species of CVDs, coronary heart disease (CHD) is becoming more and more common. The pathogenesis of CHD, especially at the molecular level, is not entirely clear up to now. Explaining the pathogenesis of CHD is particularly important for its treatment and prognosis. Biological database data analysis via bioinformatics has been an important method for studying gene expression strategy in multiple human disease. The aim of this study was to identify key different expressed genes (DEGs) in CHD and elucidate the biological process of it.Methods: A total of two published microarray datasets of CHD was downloaded from the Gene Expression Omnibus (GEO). Then, bioinformatics analyses including differentially expressed genes (DEGs) analysis, venn analysis, gene ontology (GO) annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, protein and protein interaction (PPI) network construction was performed. Quantitative real-time polymerase chain reactions (RT-qPCR) were used to detect the expression levels of DEGs in CHD.Results: A total of 122 dysregulated genes were selected as DEGs in CHD. The GO annotation analysis displayed these DEGs involved in DNA transcription and mRNA splicing regulation. The DEGs regulatory network showed the downregulated genes LUC7L3, HNRNPA1, SF3B1, ARGLU1, SRSF5, SRSF11, SREK1, PNISR, DIDO1, ZRSR2 and NKTR were located in the network control center, which were the spliceosome related genes. The RT-qPCR results were consistent with our microarray analysis.Conclusion: The abnormal regulation of spliceosome might be a key factor in the development of CHD, which must play key roles in cardiovascular disease (CVD), especially in CHD. Our study has provided a new idea for the treatment and prognosis of CHD, and the spliceosome might be the potential prognostic biomarkers of it.

scholarly journals A male-specific association between AGTR1 hypermethylation and coronary heart disease

2019 ◽  
Author(s):  
Xiaojing Li ◽  
Nan Wu ◽  
Huihui Ji ◽  
Yi Huang ◽  
Haochang Hu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Data Mining ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cancer Genomics ◽  
Gene Expression Omnibus ◽  
Inverse Association ◽  
Angiotensin Ii Receptor ◽  
Specific Pcr ◽  
Data Mining Analysis

The AGTR1 gene encodes angiotensin II receptor type 1, which is involved in cardiovascular diseases such as coronary heart disease (CHD). In the current study, we analyzed AGTR1 methylation level in a Han Chinese population by SYBR green-based quantitative methylation-specific PCR (qMSP). We collected blood samples from 761 CHD patients and 398 non-CHD controls at the Ningbo First Hospital. A data mining analysis was also performed to explore the association between AGTR1 methylation and AGTR1 gene expression, using datasets from the cBioPortal for Cancer Genomics and the Gene Expression Omnibus (GEO) database. Our results showed a significantly higher percentage of methylated reference (PMR) of AGTR1 in male CHD patients compared with male non-CHD controls (median PMR: 2.12% vs. 0.59%, p = 0.037). The data mining analysis showed that AGTR1 expression was significantly increased in human hepatoma HepG2 cells treated with the demethylation agent 5-aza-2'-deoxycytidine (fold = 3.12, p = 0.009). Further data mining analysis using the cholangiocarcinoma (TCGA, PanCancer Atlas) data indicated an inverse association between AGTR1 methylation and AGTR1 expression (r = -0.595, p = 1.29E-04). Overall, our results suggest that AGTR1 methylation is involved in the regulation of AGTR1 gene expression and that AGTR1 hypermethylation is associated with CHD in males. These findings may provide new clues about the pathogenesis of CHD.

scholarly journals The antioxidant paradox: Damage and defence

2006 ◽  
Vol 28 (5) ◽  
pp. 9-12
Author(s):  
David A. Bender
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Vitamin E ◽  
Epidemiological Studies ◽  
Plasma Lipoproteins ◽  
Radical Chain ◽  
Chain Reactions ◽  
Key Factor ◽  
Intervention Trials ◽  
Radical Damage

Over the last three decades, a considerable body of evidence has accumulated to suggest that a key factor in the development of both cancer and coronary heart disease is damage to tissues or plasma lipoproteins caused by free radicals. The majority of radicals that damage tissues are reactive oxygen species, and compounds that can quench potentially damaging radical chain reactions are therefore generally referred to as antioxidants. Epidemiological studies have shown a negative correlation between intakes of antioxidants (especially vitamin E and -carotene) and the incidence of cancer and coronary heart disease, and a positive correlation between markers of radical damage and disease. At the molecular level, there are sound theories to explain how radical damage can lead to cancer and coronary heart disease, and how antioxidants may provide protection. However, the results of intervention trials of vitamin E and -carotene have been, at best, disappointing; indeed, many trials have shown increased death among people taking supposedly protective antioxidant supplements. This is the antioxidant paradox.

Leptin Gene Expression In Males Epicardial Adipose Tissue In Coronary Heart Disease

2019 ◽  
Vol 287 ◽  
pp. e254-e255
Author(s):  
E. Polyakova ◽  
O. Berkovich ◽  
O. Belyaeva ◽  
V. Ionin ◽  
E. Baranova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Coronary Heart Disease ◽  
Adipose Tissue ◽  
Heart Disease ◽  
Epicardial Adipose Tissue

scholarly journals Gene Expression Signatures of Coronary Heart Disease

2013 ◽  
Vol 33 (6) ◽  
pp. 1418-1426 ◽  
Author(s):  
Roby Joehanes ◽  
Saixia Ying ◽  
Tianxiao Huan ◽  
Andrew D. Johnson ◽  
Nalini Raghavachari ◽  
...  
Keyword(s):  
Gene Expression ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Gene Expression Signatures

scholarly journals The Difference of ACE and ACE2 Gene Expression in Patients With Acute Aortic Dissection and Coronary Heart Disease

2021 ◽  
Author(s):  
Yang Li ◽  
Long Mao ◽  
Zongwei Xiao ◽  
Sandeep Bhushan
Keyword(s):  
Gene Expression ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Arterial Wall ◽  
Acute Aortic Dissection ◽  
Venous Blood ◽  
Control Group ◽  
The Difference ◽  
Group 2 ◽  
Ace2 Gene

Abstract BackgroundTo explore whether there is a difference in the expression of ACE and ACE2 genes in patients with acute AD and CHD. MethodsBlood samples from 68 patients, including 34 cases of acute AD (including Stanford type A and B), 21 cases of CHD, and 13 cases of control group. 2 ml of venous blood is submitted for plasma ACE concentration. The arterial wall tissue was taken during the operation for mRNA detection. ResultsThe ACE concentration in the AD group was (17.9 ± 7. 9) U / L, in the CHD group was (33.5 ± 8.1) U / L, and the ACE concentration in the control group was (38.4) ±4.8) U/L, statistically significant (P<0.05). The expression of ACE gene in the AD group was (0.2265 ± 0.3783); the expression in the CHD group was (7.085 7 ± 7.692 9), with significant (P < 0. 05). The expression of ACE2 gene in the AD group was (0.766 2 ± 0.858 6); in the CHD group was (9.612 7 ± 11.542 6), and the difference was significant (P < 0. 05). The expression of the ratio of ACE / ACE2 in the AD group was (0.413 8 ± 0.448); the expression in the CHD group was (0.811 1 ± 0.256 3), the difference was statistically significant (P <0. 001). ConclusionPlasma ACE concentration, ACE and ACE2 gene expression are significantly reduced in acute AD. The imbalance of ACE and ACE2 expression may be involved in the pathogenesis of AD.

scholarly journals Adiponectin gene expression in local fat depots in patients with coronary heart disease depending on the degree of coronary lesion

2020 ◽  
Vol 92 (4) ◽  
pp. 23-29
Author(s):  
E. V. Belik ◽  
O. V. Gruzdeva ◽  
O. E. Akbasheva ◽  
Yu. A. Dyleva ◽  
D. A. Borodkina ◽  
...  
Keyword(s):  
Gene Expression ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Atherosclerotic Lesion ◽  
Syntax Score ◽  
Moderate Degree ◽  
Adiponectin Gene ◽  
Perivascular Adipose Tissue ◽  
Coronary Lesion ◽  
Fat Depots

Aim. To determine the dependence of adiponectin gene expression by subcutaneous, epicardial and perivascular adipocytes on the degree of coronary lesion in coronary heart disease. Materials and methods. 84 patients with coronary artery disease were examined. Of these, 39 people showed a moderate degree of atherosclerotic lesion of the coronary bed (less than or equal to 22 points) on the SYNTAX Score scale, 20 severe (2231 points), and 25 extremely severe (more than 32 points). Upon admission to the hospital, all patients underwent an echocardiographic study (Echocardiography, Acuson, Germany) with the calculation of the ejection fraction (EF) of the left ventricle (LV) to assess its systolic function. During a planned surgical intervention (coronary bypass surgery, CABG), adipocytes of subcutaneous, epicardial (EAT) and perivascular adipose tissue (PVAT) were taken. Adiponectin gene expression was evaluated by polymerase chain reaction (real-time PCR) using TaqMan probes. Statistical analysis was performed using Statistica 9.0. Results. The maximum level of adiponectin expression was detected in adipocytes of PVAT, and the minimum EAT. With an increase in the degree of atherosclerotic lesion of the coronary bed, the expression of the adiponectin gene in adipocytes of local depots significantly decreases r=-0.82; p=0.023. Moreover, the low level of gene expression in EAT correlated with a decrease in LV EF by r=0.73; p=0.03. In adipocytes of subcutaneous and especially PVAT, gene expression was the highest in patients with a moderate degree of coronary lesion. Conclusions. Low adiponectin gene expression in EAT is associated with an increase in the degree of atherosclerotic lesion of the coronary bed and a decrease in LV EF.

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