OBJECTIVE: Myocardial ischaemia/reperfusion (MI/R) injury is characterized by metabolic and ultrastructural changes, which lead to irreversible injury. Several mechanisms have been postulated for the pathogenesis of MI/R injury although little is known regarding the role of myocardial gene expression. METHODS AND RESULTS: In this study, suppression subtractive hybridization (SSH) was employed to systematically isolate and screen the differentially expressed genes in the MI/R injury rat model. The characteristics of these specific genes were analysed using bioinformatics. Our results showed that among the 119 identified genes, 54 genes were expressed at higher levels and 65 genes were at lower levels compared with the control group. CONCLUSIONS: These genes are closely associated with energy metabolism, iron transport, signalling transduction and may provide important clues for the elucidation of the mechanisms of MI/R injury. Our results further indicated that myocardial injury is likely the result of summation of functional impairment of multiple genes rather than the result of damage to a single critical gene.
OBJECTIVE:Myocardial ischaemia/reperfusion (MI/R) injury is characterized by metabolic and ultrastructural changes, which lead to irreversible injury. Several mechanisms have been postulated for the pathogenesis of MI/R injury although little is known regarding the role of myocardial gene expression. METHODS AND RESULTS: In this study, suppression subtractive hybridization (SSH) was employed to systematically isolate and screen the differentially expressed genes in the MI/R injury rat model. The characteristics of these specific genes were analysed using bioinformatics. Our results showed that among the 119 identified genes, 54 genes were expressed at higher levels and 65 genes were at lower levels compared with the control group. CONCLUSIONS: These genes are closely associated with energy metabolism, iron transport, signalling transduction and may provide important clues for the elucidation of the mechanisms of MI/R injury. Our results further indicated that myocardial injury is likely the result of summation of functional impairment of multiple genes rather than the result of damage to a single critical gene.