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In Vitro Model of Coronary Angiogenesis
Published on: March 10, 2020
Study of the Association between VEGF Polymorphisms and the Risk of Coronary Artery Disease in Koreans
Eun-Ju Ko1, In-Jai Kim2, Jeong-Yong Lee1
1Department of Biomedical Science, College of Life Science, CHA University, Seongnam 13488, Korea.
Insights
Genetic variations in vascular endothelial growth factor (VEGF) are linked to coronary artery disease (CAD) risk in Koreans. Specific VEGF allele combinations were associated with decreased or increased CAD prevalence, highlighting gene-environment interactions.
Area of Science:
- Genetics
- Cardiovascular Disease Research
- Molecular Biology
Background:
- Coronary artery disease (CAD) is a major global health concern with complex genetic and environmental causes.
- Vascular endothelial growth factor (VEGF) plays a crucial role in blood vessel formation and maintenance.
- The specific impact of VEGF gene polymorphisms on CAD susceptibility in the Korean population remains largely uncharacterized.
Purpose of the Study:
- To investigate the association between specific polymorphisms in the VEGF gene promoter and 3′-untranslated region (3′-UTR) and the risk of developing CAD in Koreans.
- To analyze the combined effects of VEGF polymorphisms and clinical risk factors on CAD prevalence.
Main Methods:
- Genotyping of 6 VEGF polymorphisms (2 promoter, 4 3′-UTR) in 885 Korean subjects (463 CAD patients, 422 controls) using PCR-RFLP and TaqMan assays.
- Statistical analysis including genotype frequency calculation, haplotype analysis, and genotype combination analysis.
- Gene-environment interaction analysis examining the combined impact of VEGF genotypes and clinical variables (BMI, HbA1c, LDL-C) on CAD risk.
Main Results:
- Significant associations were found between specific VEGF allele combinations and CAD susceptibility.
- The VEGF allele combination -1154A/+936T was associated with a reduced prevalence of CAD (AOR = 0.077, p = 0.021).
- Conversely, VEGF allele combinations -1498T/+1725A and -1498T/+1612A/+1725A were linked to an increased prevalence of CAD (AOR = 1.602, p = 0.047; AOR = 1.582, p = 0.045).
- Gene-environment analysis revealed that the VEGF +1725AA genotype, in conjunction with factors like BMI, HbA1c, and LDL-C, elevated CAD risk.
Conclusions:
- Specific VEGF gene polymorphisms and their combinations significantly influence CAD susceptibility in the Korean population.
- Interactions between VEGF genotypes and clinical factors like obesity and dyslipidemia contribute to the overall risk of developing CAD.
- These findings underscore the importance of considering both genetic predisposition and environmental factors in understanding and managing CAD.
Abstract:
Coronary artery disease (CAD), a leading cause of death worldwide, has a complex etiology comprising both traditional risk factors (type 2 diabetes, dyslipidemia, arterial hypertension, and cigarette smoking) and genetic factors. Vascular endothelial growth factor (VEGF) notably contributes to angiogenesis and endothelial homeostasis. However, little is known about the relationship between CAD and VEGF polymorphisms in Koreans. The aim of this study is to investigate the associations of 2 VEGF promoter region polymorphisms (−1154G>A [rs1570360], −1498T>C [rs833061]) and 4 VEGF 3′-UTR polymorphisms (+936C>T [rs3025039], +1451C>T [rs3025040], +1612G>A [rs10434], and +1725G>A [rs3025053]) with CAD susceptibility in Koreans. We studied 885 subjects: 463 CAD patients and 422 controls. Genotyping was conducted with polymerase chain reaction-restriction fragment length polymorphism analysis and TaqMan allelic discrimination assays, and the genotype frequencies were calculated. We then performed haplotype and genotype combination analyses and measured the associations between VEGF polymorphisms and clinical variables in both the CAD patients and control subjects. We detected statistically significant associations between CAD and certain VEGF allele combinations. In the haplotypes of 5 single-nucleotide polymorphisms, the VEGF allele combination −1154A/+936T was associated with a decreased prevalence of CAD (A-T-T-G-G of VEGF −1154G>A/−1498T>C/+936C>T/+1612G>A/+1725G>A, AOR = 0.077, p = 0.021). In contrast, the VEGF allele combinations −1498T/+1725A and −1498T/+1612A/+1725A were associated with an increased prevalence of CAD (G-T-C-C-A of VEGF −1154G>A/−1498T>C/+936C>T/+1451C>T/+1725G>A, AOR = 1.602, p = 0.047; T-C-C-A-A of VEGF −1498T>C/+936C>T/+1451C>T/+1612G>A/+1725G>A, AOR = 1.582, p = 0.045). Gene−environment combinatorial analysis showed that the combination of the VEGF +1725AA genotype and several clinical factors (e.g., body mass index, hemoglobin A1c, and low-density lipoprotein cholesterol) increased the risk of CAD. Therefore, we suggest that VEGF polymorphisms and clinical factors may impact CAD prevalence.
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