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Disparity of gene expression in coronary artery disease: insights from MEIS1, HIRA, and Myocardin.

Authors :
Javanshir, Elnaz
Ebrahimi, Zahra Javadpour
Mirzohreh, Seyedeh Tarlan
Ghaffari, Samad
Banisefid, Erfan
Alamdari, Naimeh Mesri
Roshanravan, Neda
Source :
Molecular Biology Reports; 6/1/2024, Vol. 51 Issue 1, p1-10, 10p
Publication Year :
2024

Abstract

Introduction: Coronary artery disease (CAD) in young adults can have devastating consequences. The cardiac developmental gene MEIS1 plays important roles in vascular networks and heart development. This gene effects on the regeneration capacity of the heart. Considering role of MEIS1 in cardiac tissue development and the progression of myocardial infarction this study investigated the expression levels of the MEIS1, HIRA, and Myocardin genes in premature CAD patients compared to healthy subjects and evaluated the relationships between these genes and possible inflammatory factors. Methods and results: The study conducted a case-control design involving 35 CAD patients and 35 healthy individuals. Peripheral blood mononuclear cells (PBMCs) were collected, and gene expression analysis was performed using real-time PCR. Compared with control group, the number of PBMCs in the CAD group exhibited greater MEIS1 and HIRA gene expression, with fold changes of 2.45 and 3.6. The expression of MEIS1 exhibited a negative correlation with IL-10 (r= -0.312) expression and positive correlation with Interleukin (IL)-6 (r = 0.415) and tumor necrosis factor (TNF)-α (r = 0.534) gene expression. Moreover, there was an inverse correlation between the gene expression of HIRA and that of IL-10 (r= -0.326), and a positive correlation was revealed between the expression of this gene and that of the IL-6 (r = 0.453) and TNF-α (r = 0.572) genes. Conclusion: This research demonstrated a disparity in expression levels of MEIS1, HIRA, and Myocardin, between CAD and healthy subjects. The results showed that, MEIS1 and HIRA play significant roles in regulating the synthesis of proinflammatory cytokines, namely, TNF-α and IL-6. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
03014851
Volume :
51
Issue :
1
Database :
Complementary Index
Journal :
Molecular Biology Reports
Publication Type :
Academic Journal
Accession number :
177596483
Full Text :
https://doi.org/10.1007/s11033-024-09657-5