Abstract
BackgroundModern fast-growing broilers are susceptible to heart failure under heat stress because their relatively small hearts cannot meet increased need of blood pumping. To improve the cardiac tolerance to heat stress in modern broilers through breeding, we need to find the important genes and pathways that contribute to imbalanced cardiac development and frequent occurrence of heat-related heart dysfunction. Two broiler lines – Ross 708 and Illinois – were included in this study as a fast-growing model and a slow-growing model respectively. Each broiler line was separated to two groups at 21 days posthatch. One group was subjected to heat stress treatment in the range of 35–37 °C for 8 h per day, and the other was kept in thermoneutral condition. Body and heart weights were measured at 42 days posthatch, and gene expression in left ventricles were compared between treatments and broiler lines through RNA-seq analysis.ResultsBody weight and normalized heart weight were significantly reduced by heat stress only in Ross broilers. RNA-seq results of 44 genes were validated using Biomark assay. A total of 325 differentially expressed (DE) genes were detected between heat stress and thermoneutral in Ross 708 birds, but only 3 in Illinois broilers. Ingenuity pathway analysis (IPA) predicted dramatic changes in multiple cellular activities especially downregulation of cell cycle. Comparison between two lines showed that cell cycle activity is higher in Ross than Illinois in thermoneutral condition but is decreased under heat stress. Among the significant pathways (P < 0.01) listed for different comparisons, “Mitotic Roles of Polo-like Kinases” is always ranked first.ConclusionsThe increased susceptibility of modern broilers to cardiac dysfunction under heat stress compared to slow-growing broilers could be due to diminished heart capacity related to reduction in relative heart size. The smaller relative heart size in Ross heat stress group than in Ross thermoneutral group is suggested by the transcriptome analysis to be caused by decreased cell cycle activity and increased apoptosis. The DE genes in RNA-seq analysis and significant pathways in IPA provides potential targets for breeding of heat-tolerant broilers with optimized heart function.
Highlights
Modern fast-growing broilers are susceptible to heart failure under heat stress because their relatively small hearts cannot meet increased need of blood pumping
When we did a post-hoc least significant difference (LSD) test, we found a significant decrease of body weight and relative heart weight induced by the
After exposure to heat stress for 21 days, Ross broilers showed a significant decrease in normalized heart weight (P < 0.05), while Illinois broilers did not change (Fig. 1b) compared to the thermoneutral group, indicating that the heart weight decreased faster than that of body weight (BW) in Ross broilers under heat stress, but did not change significantly in Illinois broilers
Summary
Modern fast-growing broilers are susceptible to heart failure under heat stress because their relatively small hearts cannot meet increased need of blood pumping. Changes in the cardiovascular system usually occurred to acclimate long-term thermal environment Such thermoregulatory response can only enable them survive within a limited range of thermal zone at the sacrifice of food production, despite the varied tolerance to heat stress between different animals [1]. Modern broilers with fast growth rate are susceptible to cardiac dysfunction due to small hearts relative to large body size. To initiate the breeding of broilers resistant to heat stress and heart failure, it is important to identify significant genes and pivotal pathways responsible for the increased susceptibility to cardiac dysfunction and sensitivity to heat stress in fast-growing broilers compared to slow-growing broilers
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