Volume 15, Issue 2 (6-2024)
Res Anim Prod 2024, 15(2): 21-31 |
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Badakhshan Y, Roudbari Z. (2024). Effects of Cyclic-Chronic Heat Stress on Contractility-Related Genes in the Heart Muscle of Broilers based on RNA-Seq. Res Anim Prod. 15(2), 21-31. doi:10.61186/rap.15.2.21
URL: http://rap.sanru.ac.ir/article-1-1392-en.html
URL: http://rap.sanru.ac.ir/article-1-1392-en.html
1- Department of Animal Science, Faculty of Agriculture, University of Jiroft, Jiroft, Iran & Department of Animal Science, Faculty of Agriculture, University of Jiroft, Jiroft, Iran
Abstract: (1382 Views)
Extended Abstract
Background: Rapid growth of broilers leads to insufficient cardiac output, cardiac hypertrophy, and finally sudden death. When livestock are exposed to hot environments, they often try to dissipate heat by increasing blood flow to the skin. This physiological response is a way for animals to adapt to long-term thermal conditions. However, this thermoregulatory mechanism has its limitations. While different animals have varying degrees of tolerance to heat stress, the cardiovascular system can only compensate within a certain range before it starts to impact food production. Domestic poultry, such as chickens, lack sweat glands, which is a key mechanism for body cooling in many other animals. This deficiency forces the cardiovascular system to work harder, sending more blood to the skin to help regulate body temperature. Broilers, in particular, have a narrow thermoneutral zone (the range of temperatures where an animal can maintain its body temperature without expending extra energy) and a high metabolic rate, which places an even greater burden on their cardiac function. Therefore, it is an appropriate model for studying cardiac disease. Heat stress is among the stressors affecting cardiac performance. In accordance with the cardiac system susceptibility of poultry to heat stress, especially broilers because of their fast growth rate, to enhance the ability of modern broiler chickens to withstand heat stress through selective breeding, we need to identify the crucial genes and biological processes that lead to unbalanced heart development and the high incidence of heat-induced heart problems. Thus, the aim was to consider the gene expression of cardiac contractility proteins under heat stress conditions during the growing period of broilers.
Methods: Ross 708 broilers were subjected to heat stress (HS) of 35–37 °C for 8 hours daily for 21 days post-hatch. Initially, male broilers had unrestricted access to feed and water in spacious colony houses maintained at 33 °C, with the temperature gradually decreasing by 3 °C per week until it reached 24 °C by the day 21 post-hatch. At the conclusion of the growth period, the broilers were euthanized, and their left ventricles were isolated for mRNA extraction. RNA-seq data were obtained from NCBI’s with the accession number SRP082125. All the expressions of deferentially expressed genes (DEGs) were determined and analyzed by DAVID online bioinformatics tools. Gene ontology qualification, including biological processes (BP), cellular component (CC), and molecular role (MF), were achieved from DAVID. Heat stress induction was from days 21-42 for 8 hours every day for 21 days until to end of the growing period.
Results: Gene expression changes were related to 35 genes of the muscular cardiocyte of the left ventricle. From seven genes related to the protein of troponin, TNN and TNNI1 genes, declined significantly, with an increase in the TNNT3 gene expression (P< 0.05). Of five genes related to the tropomyosin protein, the TPM1 gene showed a significant increase in expression (P < 0.05). Of the two genes related to the ryanodine receptor, RYR3 had significant gene upregulation (P < 0.05). From the ten genes related to DHPR, only CACNA2D2 had significant downregulation (P < 0.05). Among four calmodulin-related genes, CAMKK1 and CAMK1D showed significant downregulation, and CAMSAP2 revealed upregulation (P< 0.05). Significant reductions occurred in the expression of five associated genes of heavy-chain myosin (P< 0.05).
Conclusion: Heat stress reduced gene expression of ryanodine, DHPR, and troponin, those related to calcium release into the cell cytosol. Furthermore, it prevents cardiac hypertrophy by decreasing the expression of genes related to the heavy chain of myosin. Thus, the vulnerability of modern broilers to heart problems, when exposed to high temperatures, may be linked to their heart's reduced capacity, which is likely due to their relatively smaller heart size. According to genetic analysis, the smaller heart size in broilers under heat stress than those in a comfortable temperature environment is likely caused by slower cell growth and division. This research identifies specific genes and biological pathways that could be targeted through breeding to develop broilers that are more resistant to heat stress and have healthier hearts. This study has identified specific genes and biological processes linked to the reduction in heart size observed in broiler chickens subjected to heat stress. These insights provide new opportunities for developing targeted breeding strategies to address this issue. The findings indicate that selective breeding, by focusing on the identified genes and pathways, may enable the development of broiler chickens that are more resistant to heat stress and have healthier hearts. By concentrating on these genetic factors, breeders can work toward creating broiler populations that are more resilient to high temperatures and less susceptible to heart problems.
Background: Rapid growth of broilers leads to insufficient cardiac output, cardiac hypertrophy, and finally sudden death. When livestock are exposed to hot environments, they often try to dissipate heat by increasing blood flow to the skin. This physiological response is a way for animals to adapt to long-term thermal conditions. However, this thermoregulatory mechanism has its limitations. While different animals have varying degrees of tolerance to heat stress, the cardiovascular system can only compensate within a certain range before it starts to impact food production. Domestic poultry, such as chickens, lack sweat glands, which is a key mechanism for body cooling in many other animals. This deficiency forces the cardiovascular system to work harder, sending more blood to the skin to help regulate body temperature. Broilers, in particular, have a narrow thermoneutral zone (the range of temperatures where an animal can maintain its body temperature without expending extra energy) and a high metabolic rate, which places an even greater burden on their cardiac function. Therefore, it is an appropriate model for studying cardiac disease. Heat stress is among the stressors affecting cardiac performance. In accordance with the cardiac system susceptibility of poultry to heat stress, especially broilers because of their fast growth rate, to enhance the ability of modern broiler chickens to withstand heat stress through selective breeding, we need to identify the crucial genes and biological processes that lead to unbalanced heart development and the high incidence of heat-induced heart problems. Thus, the aim was to consider the gene expression of cardiac contractility proteins under heat stress conditions during the growing period of broilers.
Methods: Ross 708 broilers were subjected to heat stress (HS) of 35–37 °C for 8 hours daily for 21 days post-hatch. Initially, male broilers had unrestricted access to feed and water in spacious colony houses maintained at 33 °C, with the temperature gradually decreasing by 3 °C per week until it reached 24 °C by the day 21 post-hatch. At the conclusion of the growth period, the broilers were euthanized, and their left ventricles were isolated for mRNA extraction. RNA-seq data were obtained from NCBI’s with the accession number SRP082125. All the expressions of deferentially expressed genes (DEGs) were determined and analyzed by DAVID online bioinformatics tools. Gene ontology qualification, including biological processes (BP), cellular component (CC), and molecular role (MF), were achieved from DAVID. Heat stress induction was from days 21-42 for 8 hours every day for 21 days until to end of the growing period.
Results: Gene expression changes were related to 35 genes of the muscular cardiocyte of the left ventricle. From seven genes related to the protein of troponin, TNN and TNNI1 genes, declined significantly, with an increase in the TNNT3 gene expression (P< 0.05). Of five genes related to the tropomyosin protein, the TPM1 gene showed a significant increase in expression (P < 0.05). Of the two genes related to the ryanodine receptor, RYR3 had significant gene upregulation (P < 0.05). From the ten genes related to DHPR, only CACNA2D2 had significant downregulation (P < 0.05). Among four calmodulin-related genes, CAMKK1 and CAMK1D showed significant downregulation, and CAMSAP2 revealed upregulation (P< 0.05). Significant reductions occurred in the expression of five associated genes of heavy-chain myosin (P< 0.05).
Conclusion: Heat stress reduced gene expression of ryanodine, DHPR, and troponin, those related to calcium release into the cell cytosol. Furthermore, it prevents cardiac hypertrophy by decreasing the expression of genes related to the heavy chain of myosin. Thus, the vulnerability of modern broilers to heart problems, when exposed to high temperatures, may be linked to their heart's reduced capacity, which is likely due to their relatively smaller heart size. According to genetic analysis, the smaller heart size in broilers under heat stress than those in a comfortable temperature environment is likely caused by slower cell growth and division. This research identifies specific genes and biological pathways that could be targeted through breeding to develop broilers that are more resistant to heat stress and have healthier hearts. This study has identified specific genes and biological processes linked to the reduction in heart size observed in broiler chickens subjected to heat stress. These insights provide new opportunities for developing targeted breeding strategies to address this issue. The findings indicate that selective breeding, by focusing on the identified genes and pathways, may enable the development of broiler chickens that are more resistant to heat stress and have healthier hearts. By concentrating on these genetic factors, breeders can work toward creating broiler populations that are more resilient to high temperatures and less susceptible to heart problems.
Type of Study: Research |
Subject:
ژنتیک و اصلاح نژاد دام
Received: 2023/06/6 | Accepted: 2023/12/10
Received: 2023/06/6 | Accepted: 2023/12/10
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