Dynamic expression of early responsible genes to acute left-ventricular ischemia in a time-dependent pattern

• Published in: Animal cells and systems Vol. 18; no. 3; pp. 190 - 196
• Main Authors: Song, XiaoWei, Shen, Ya Feng, Cao, Mi, Yuan, QingNing, Tang, Ying, Lei, Changhai, Yang, Yong Ji
• Format: Journal Article
• Language: Korean
• Published: 2014
• Subjects: IL6; ANP; TNF{\alpha}; C-Myc; acute myocardial infarction; SOD1
• ISSN: 1976-8354; 2151-2485

Acute myocardial infarction remains one of the leading causes of death and disability worldwide. The mechanisms underlying myocardial infarction involve a complex of signaling molecules, such as tumor necrosis factor ${\alpha}$ ($TNF{\alpha}$), interleukin-6 (IL6), C-Myc, atria natriuretic peptide (ANP), superoxide dismutase 1 (SOD1), and so on. The aim of this study is to understand the time-dependent expressional pattern of these early responsible genes following acute myocardial ischemia established by left anterior descending (LAD) coronary artery ligation. After LAD ligation, a collection of genes was detected using real-time polymerase chain reaction (PCR). The expression of inflammation-related genes, such as $TNF{\alpha}$ and IL6, was immediately upregulated at 2 h, reached to the highest point at 12 h, and then decreased to nearly basis level at 24 h after ligation, suggesting inflammation appeared and disappeared rapidly after acute ischemia. C-Myc, an important transcription factor, was significantly upregulated at 2 h, and thereafter persisted at high level to 24 h. The secretary peptide, ANP, was consistently upregulated from 2 to 24 h, reached to 40-folds at 24 h. The calcium-regulated gene, FK506-binding protein 12.6, was not significantly altered after ischemia. SOD1 was not altered at the first 4 h, and began to downregulate at 12 and 24 h. These results indicate that several genes were dynamically and transiently regulated after acute myocardial infarction (AMI) in a time-dependent pattern, suggesting that there is an immediate molecular response to acute myocardial ischemia, which might provide us a new insight to understand molecular mechanisms of AMI.