Assistant professor Department of Animal Science, Faculty of Agriculture, University of Jiroft, Jiroft, Iran & Assistant professor Department of Animal Science, Faculty of Agriculture, University of Jiroft, Jiroft, Iran
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Extended Abstract
Introduction and objective: Rapid growth of Broiler led 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.. There by it is an appropriate model for cardiac disease studying. Heat stress is one of affective stressor on cardiac performance. in accordance to cardiac system susceptibility of poultry to heat stress, specially broiler 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 cardiac contractility proteins gene expression under heat stress condition during growing period of broilers.
Material and Methods: Ross 708 broilers were subjected to heat stress (HS) between 35–37 °C for 8 hours daily for 21 days posthatch. Initially, the male broilers had unrestricted access to feed and water in spacious colony houses maintained at 33 °C, with the temperature gradually decreased by 3 °C per week until it reached 24 °C by the 21st day posthatch. 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 accession number SRP082125 All the expression of deferentially expressed genes (DEGs) were determined and analyzed by DAVID online bioinformatic tools. Gene ontology qualification including biological processes (BP), cellular component (CC), and molecular role (MF) were achieved from DAVID. Heat stress induction was from day 21-42 for 8 hours every day for 21 days until to end of growing period.
Results: Gene expression changes were related to 35 genes of muscular cardiocyte of left ventricle. From seven gene-related to protein of troponin, TNN, TNNI1 genes had significantly reduction and TNNT3 increase gene expression respectively (P<0.05). five genes related to tropomyosin protein, TPM1 gene showed significant increase in gene expression (P<0.05). between two gene-related to ryanodine receptor, RYR3 had significant gene up regulation (P<0.05). from ten gene-related to DHPR only CACNA2D2 had significant down regulation (P<0.05). four calmodulin-related genes, CAMKK1, CAMK1D showed significant down and CAMSAP2 up regulation (P<0.05). expression of five associated genes of heavy-chain myosin significantly reduced (P<0.05).
Conclusion: in conclusion, heat stress reduced gene expression of ryanodine, DHPR and troponin, those related to calcium release into cytosol of cell. Furthermore prevented cardiac hypertrophy by decrease in expression of genes related to 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 compared to 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, 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 towards creating broiler populations that are more resilient to high temperatures and less susceptible to heart problems.
Introduction and objective: Rapid growth of Broiler led 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.. There by it is an appropriate model for cardiac disease studying. Heat stress is one of affective stressor on cardiac performance. in accordance to cardiac system susceptibility of poultry to heat stress, specially broiler 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 cardiac contractility proteins gene expression under heat stress condition during growing period of broilers.
Material and Methods: Ross 708 broilers were subjected to heat stress (HS) between 35–37 °C for 8 hours daily for 21 days posthatch. Initially, the male broilers had unrestricted access to feed and water in spacious colony houses maintained at 33 °C, with the temperature gradually decreased by 3 °C per week until it reached 24 °C by the 21st day posthatch. 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 accession number SRP082125 All the expression of deferentially expressed genes (DEGs) were determined and analyzed by DAVID online bioinformatic tools. Gene ontology qualification including biological processes (BP), cellular component (CC), and molecular role (MF) were achieved from DAVID. Heat stress induction was from day 21-42 for 8 hours every day for 21 days until to end of growing period.
Results: Gene expression changes were related to 35 genes of muscular cardiocyte of left ventricle. From seven gene-related to protein of troponin, TNN, TNNI1 genes had significantly reduction and TNNT3 increase gene expression respectively (P<0.05). five genes related to tropomyosin protein, TPM1 gene showed significant increase in gene expression (P<0.05). between two gene-related to ryanodine receptor, RYR3 had significant gene up regulation (P<0.05). from ten gene-related to DHPR only CACNA2D2 had significant down regulation (P<0.05). four calmodulin-related genes, CAMKK1, CAMK1D showed significant down and CAMSAP2 up regulation (P<0.05). expression of five associated genes of heavy-chain myosin significantly reduced (P<0.05).
Conclusion: in conclusion, heat stress reduced gene expression of ryanodine, DHPR and troponin, those related to calcium release into cytosol of cell. Furthermore prevented cardiac hypertrophy by decrease in expression of genes related to 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 compared to 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, 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 towards 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 | Revised: 2023/12/9 | Accepted: 2023/12/10
Received: 2023/06/6 | Revised: 2023/12/9 | Accepted: 2023/12/10
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