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Chronic heat stress causes liver damage via endoplasmic reticulum stress-induced apoptosis in broilers.

ABSTRACT: Liver is a central metabolic organ, which is sensitive to heat stress. Liver damage affects animals' health and endangers the livestock and poultry industry. This study aimed to investigate the mechanism of chronic heat stress-induced liver damage in broiler chickens. Broilers were divided into 3 treatments: normal control group (NOR, 22°C), heat stress group (HS, 32°C) and pair-feeding group (PF, 22°C) for a 7-d and 14-d trial. The results showed that 7 d heat exposure caused microvesicular steatosis and reduced glutamine synthetase activity in broiler liver (P < 0.05). After 14 d of heat exposure, heat stress caused vacuolar degeneration and apoptosis in the liver; elevated liver relative weight and liver glutaminase activity as well as plasma ammonia level (P < 0.05). Additionally, heat stress enhanced GRP78 protein expression and the mRNA expressions of endoplasmic reticulum (ER) stress responses genes and apoptosis-related genes in broiler liver after 14 d of heat exposure (P < 0.05). In conclusion, chronic heat stress triggered ER stress-induced apoptosis and caused liver damage, which may compromise ammonia detoxification in broiler liver.

SUBMITTER: Ma B

PROVIDER: S-EPMC9445382 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

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Chronic heat stress causes liver damage via endoplasmic reticulum stress-induced apoptosis in broilers.

Ma Bingbing B Xing Tong T Li Jiaolong J Zhang Lin L Jiang Yun Y Gao Feng F

Poultry science 20220726 10

Liver is a central metabolic organ, which is sensitive to heat stress. Liver damage affects animals' health and endangers the livestock and poultry industry. This study aimed to investigate the mechanism of chronic heat stress-induced liver damage in broiler chickens. Broilers were divided into 3 treatments: normal control group (NOR, 22°C), heat stress group (HS, 32°C) and pair-feeding group (PF, 22°C) for a 7-d and 14-d trial. The results showed that 7 d heat exposure caused microvesicular ste ...[more]

PMID: 36049294

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Project description:PurposeEndoplasmic reticulum (ER) and mitochondrial stress are independently associated with corneal endothelial cell (CEnC) loss in many corneal diseases, including Fuchs' endothelial corneal dystrophy (FECD). However, the role of ER stress in mitochondrial dysfunction contributing to CEnC apoptosis is unknown. The purpose of this study is to explore the crosstalk between ER and mitochondrial stress in CEnC.MethodsHuman corneal endothelial cell line (HCEnC-21T) and human corneal endothelial tissues were treated with ER stressor tunicamycin. ER stress-reducing chemical 4-phenyl butyric acid (4-PBA) was used in HCEnC-21T after tunicamycin. Fuchs' corneal endothelial cell line (F35T) was used to determine differential activation of ER stress with respect to HCEnC-21T at the baseline. ER stress, mitochondrial-mediated intrinsic apoptotic, mitochondrial fission, and fusion proteins were determined using immunoblotting and immunohistochemistry. Mitochondrial bioenergetics were assessed by mitochondrial membrane potential (MMP) loss and ATP production at 48 hours after tunicamycin. Mitochondria dynamics (shape, area, perimeter) were also analyzed at 24 hours using transmission electron microscopy.ResultsTreatment of HCEnC-21T cell line with tunicamycin activated three ER stress pathways (PERK-eIF2α-CHOP, IRE1α-XBP1, and ATF6), reduced cell viability, upregulated mitochondrial-mediated intrinsic apoptotic molecules (cleaved caspase 9, caspase 3, PARP, Bax, cytochrome C), downregulated anti-apoptotic Bcl-2 protein, initiated mitochondrial dysfunction by loss of MMP and lowering of ATP production, and caused mitochondrial swelling and fragmentation with increased expression of mitochondrial fission proteins (Fis1 and p-Drp1). Fuchs' CEnC (F35T) cell line also showed activation of the ER stress-related proteins (p-eIF2α, GRP78, CHOP, XBP1) compared to HCEnC-21T at the baseline. The 4-PBA ameliorated cell loss and reduced cleaved caspase 3 and 9, thereby rescuing tunicamycin-induced cell death but not mitochondrial bioenergetics in HCEnC-21T cell line.ConclusionsTunicamycin-induced ER stress disrupts mitochondrial bioenegetics, dynamics and contributes to the loss of CEnC viability. This novel study highlights the importance of ER-mitochondria crosstalk and its contribution to CEnCs apoptosis, seen in many corneal diseases, including FECD.

Project description:With the increasing of global mean surface air temperature, heat stress (HS) induced by extreme high temperature has become a key factor restricting the poultry industry. Liver is the main metabolic organ of broilers, HS induces liver damage and metabolic disorders, which impairs the health of broilers and affects food safety. As an essential trace element for animals, selenium (Se) involves in the formation of antioxidant system, and its biological functions are generally mediated by selenoproteins. However, the mechanism of Se against HS induced liver damage and metabolic disorders in broilers is inadequate. Therefore, we developed the chronic heat stress (CHS) broiler model and investigated the potential protection mechanism of organic Se (selenomethionine, SeMet) on CHS induced liver damage and metabolic disorders. In present study, CHS caused liver oxidative damage, and induced hepatic lipid accumulation and glycogen infiltration of broilers, which are accompanied by mitochondrial dysfunction, abnormal mitochondrial tricarboxylic acid (TCA) cycle and endoplasmic reticulum (ER) stress. Dietary SeMet supplementation increased the hepatic Se concentration and exhibited protective effects via promoting the expression of selenotranscriptome and several key selenoproteins (GPX4, TXNRD2, SELENOK, SELENOM, SELENOS, SELENOT, GPX1, DIO1, SELENOH, SELENOU and SELENOW). These key selenoproteins synergistically improved the antioxidant capacity, and mitigated the mitochondrial dysfunction, abnormal mitochondrial TCA cycle and ER stress, thus recovered the hepatic triglyceride and glycogen concentration. What's more, SeMet supplementation suppressed lipid and glycogen biosynthesis and promoted lipid and glycogen breakdown in liver of broilers exposed to CHS though regulating the AMPK signals. Overall, our present study reveals a potential mechanism that Se alleviates environment HS induced liver damage and glycogen and lipid metabolism disorders in broilers, which provides a preventive and/or treatment measure for environment HS-dependent hepatic metabolic disorders in poultry industry.

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Chronic heat stress causes liver damage via endoplasmic reticulum stress-induced apoptosis in broilers.

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Chronic heat stress causes liver damage via endoplasmic reticulum stress-induced apoptosis in broilers.

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