Abstract
Abstract Introduction Burn-related cardiac mitochondria dysfunction (BRMD) is associated with negative health outcomes and decreased health-related quality of life; however, few studies of the molecular-genetic mechanisms of BRMD exist. Methods 60% of total body surface area (TBSA) burned rats was employed. O2K Respirometer system (Innsbruck, Austria) was utilized to measure cardiac mitochondrial function. OXPHOS complex activities were determined by using OXPHOS enzyme complex activity assays (Cayman Chemical, Ann Arbor, Michigan). The Rat Mitochondria RT2 Profiler PCR Array was used to identify differential regulation of genes involved in mitochondrial biogenesis and metabolism function. Results Burn injury induced cardiac mit dysfunction by decreasingOXPHOS oxygen consumption at State 3 energized by malate/pyruvate and succinate and declining mit ETC activity in complex I, III, IV and V. 84 rat mit-related gene profiles were measured. The mitochondrial gene profile showed that 30/84 genes related to mitochondrial function and structure were differentially expressed. Of these 30 genes, 17 (ATP12a, ATP4a, ATP6v0a2, ATP6v1e2, ATP6v1g3, COX8c, LHPP, NDUFA5, SLC25a10, SLC25a15, UCP1, UCP2, UCP3, UQCRFS1, LDHA and RGDC) were more than 2 fold up-regulated, and 13 (ATP5c1, ATP5i, ATP5L, COX17, COX6c, COX7a2, NDUFA8, NDUFB3, NDUFB7, NDUFB9, NDUFS4, NDUFS8, and UQCRB) were greater than 2-fold down-regulated. Furthermore, 8 genes (AIFM2, BCL2, FIS1, IMMP2L, MSTO1, SLC25A23, SLC25A37, SLC25A4) that had significant differentially expression were associated with heart dysfunction. Conclusions This study provides preliminary evidence that 30 mitochondrial function genes were significantly associated with burn-induced heart dysfunction in 24 hpb rats. Applicability of Research to Practice These findings elucidate possible pathways and early biomarkers for targeting novel interventions for burn-induced heart dysfunction.
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