Gene Expression Disparity in Coronary Artery Disease: Insights from MEIS1, HIRA, and Myocardin

Elnaz Javanshir, Zahra Javadpour Ebrahimi, Seyedeh Tarlan MirzohrehM,Samad Ghaffari,Erfan Banisefid,Naimeh Mesri Alamdari,Neda Roshanravan

crossref(2024)

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摘要
Abstract Introduction: Coronary artery disease (CAD) manifesting in young adults can have devastating consequences. MEIS1 gene plays an important role in vascular networks and heart development. Also, this gene has a great effect on the regeneration capacity of the heart. This study investigates the expression level of MEIS1, HIRA, and Myocardin genes in patients with premature CAD in comparison to healthy subjects and evaluates the relationship between these genes and possible inflammatory factors. Methods and Results A case-control study was employed to investigate HIRA, MEIS1, and Myocardin gene expression as well as IL-6, IL-10, and TNF-α in Peripheral Blood Mononuclear Cells (PBMCs) obtained from CAD patients. Thirty-five patients diagnosed with CAD and 35 healthy individuals enrolled through simple randomization. RNAs were extracted from PBMCs and cDNA synthesis was performed to determine the expression levels of studied genes using real-time PCR. PBMCs of CAD cases demonstrated higher levels of MEIS1 and HIRA gene expression compared to the control group with a fold change of 2.45 and 3.6 respectively. Expression of MEIS1 exhibited a negative correlation with IL-10 (r= -0.312) expression and a positive correlation with IL-6 (r = 0.415) and TNF-α (r = 0.534) gene expressions. Moreover, there was an inverse correlation between the gene expressions of HIRA and IL-10 (r= -0.326), and a positive correlation was revealed between this gene and the IL-6 (r = 0.453) and TNF-α (r = 0.572) gene expressions. Conclusion This research demonstrated a distinct disparity in the expression levels of MEIS1, HIRA, and Myocardin as early myocardial marker genes between individuals with CAD and healthy subjects. Results showed that two specific genes, MEIS1 and HIRA, may play a significant role in regulating the synthesis of pro-inflammatory cytokines, namely TNF-α and IL-6.
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