Effect of acute heat stress on adrenocorticotropic hormone, cortisol, interleukin-2, interleukin-12 and apoptosis gene expression in rats

Wang, L I; Liu, Fadong; Luo, Yan; Zhu, Li; Li, Guanghua

doi:10.3892/br.2015.445

Cited by 59 publications

(37 citation statements)

References 25 publications

(20 reference statements)

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“…In recent years, the effects of continuous high-temperature environments on animal health and well-being are gaining more attention (Maglara et al 2003;Wang et al 2015). As a source of stress, a high-temperature environment triggers a series of heat stress responses in the body.…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Chen

Shi

et al. 2016

In Vitro Cell.Dev.Biol.-Animal

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Heat stress can weaken the immune system and even increase livestock's susceptibility to disease. MicroRNA (miR) is short non-coding RNA that functions in post-transcriptional regulation of gene expression and some phenotypes. Our recent study found that miR-181a is highly expressed in the serum of heat-stressed Holstein cows, but the potential function of miR-181a is still not clarified. In this study, peripheral blood mononuclear cells (PBMCs), isolated from Holstein cows' peripheral blood, were used to investigate the effects of miR-181a inhibitor on heat stress damage. Our results showed that significant apoptosis and oxidative damage were induced by heat stress in PBMCs. However, with apoptosis, the levels of reactive oxygen species (ROS) and content of malondialdehyde (MDA) were reduced, while the content of glutathione (GSH) and the activity of superoxide dismutase (SOD) were increased even under heat stress conditions after transfecting miR-181a inhibitors to PBMCs. Meanwhile, mRNA expression of bax and caspase-3 was significantly decreased, but mRNA expression of bcl-2 was increased in transfected PBMCs. In conclusion, our results demonstrated that down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows.

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Section: Introductionmentioning

confidence: 99%

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Chen

Shi

et al. 2016

In Vitro Cell.Dev.Biol.-Animal

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“…Our first main finding is that the extracellular exosome present in blood and adrenal glands can be an important regulator of HS. Previous studies assessed the degree of HS in livestock based on physiological (e.g., body temperature [52], salivary or respiratory rate [53], and biochemical indicators (e.g., cortisol, adrenocorticotropic hormone, prolactin) [10,54]). However, the genetic background, HS intensity and duration can affect the stability and reliability of the response to HS.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, further molecular mechanisms and physiological consequences of HS using an animal model are highly recommended.Previous studies have shown HS-induced physiological and biochemical variations in many animals, such as rats [10,11], cows [12], and chickens [13]. The HS causes an imbalance of glucocorticoids, the adrenocorticotropic hormone, the growth hormone, and the norepinephrine hormone, resulting in detrimental metabolic changes [10,14,15]. Furthermore, a set of proteins involved in the antioxidant stress response and inflammatory response, including catalase, glutathione peroxidase, and C-reactive protein were affected by HS [16][17][18][19].…”

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confidence: 99%

Heat Stress Impairs the Physiological Responses and Regulates Genes Coding for Extracellular Exosomal Proteins in Rat

Dou

Khan

et al. 2020

Genes

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Heat stress (HS) is challenging in humans and animals as it is a complicated regulatory mechanism. This prompted us to characterize the physiological and molecular responses of a HS-animal model. In this study, a rat model system was developed by using three temperature treatments (40°C, 42°C, and 43°C) and sixteen biochemical indicators in blood at 42°C for 30 min (H30), 60 min (H60), and 120 min (H120). In addition, transcriptomic profiling was carried out in H120-rats' blood, liver, and adrenal gland samples for detection of the genes of interest. Our findings demonstrated that the adrenocorticotropic hormone, catalase, prolactin, growth hormone, and lactic acid have significant spatiotemporal variation in the H120-rats as compared with the control. Furthermore, through transcriptomic screening, we documented a high ratio of differentially expressed genes (DEGs) in adrenal glands, liver, and blood, respectively. Among them, Nup153, Plxnb2, Stx7, Hspa9, Chordc1, Pde4d, Gm2α, and Rnf125 were associated with the regulation of HS and immune response processes. Notably, 36 and 314 of DEGs in blood and adrenal glands were detected in the composition of the extracellular exosome, respectively. Furthermore, the correlation analysis between gene transcripts and biochemical indicator levels identified the Lgals3, S1006, Fn1, F2, and Kng1l1 as key candidate genes for HS encoding extracellular exosomal proteins. On the basis of our results, it was concluded that the current rat model provides a molecular basis for future research in HS resistance in humans and livestock.Genes 2020, 11, 306 2 of 23 (e.g., crossbreeding), have not achieved long-lasting, cumulative and significant effects [9]. Thus, further molecular mechanisms and physiological consequences of HS using an animal model are highly recommended.Previous studies have shown HS-induced physiological and biochemical variations in many animals, such as rats [10,11], cows [12], and chickens [13]. The HS causes an imbalance of glucocorticoids, the adrenocorticotropic hormone, the growth hormone, and the norepinephrine hormone, resulting in detrimental metabolic changes [10,14,15]. Furthermore, a set of proteins involved in the antioxidant stress response and inflammatory response, including catalase, glutathione peroxidase, and C-reactive protein were affected by HS [16][17][18][19]. Recently, microarray and next-generation sequencing studies have displayed widespread changes in gene expression in response to HS, the exploration of useful indicators to predict and prevent HS in animals has yet to be defined.In the context of the critical effects of HS on human and animal health, the current study was designed to explore the physiological, biochemical, and transcriptomic responses to HS in Sprague Dawley (SD) rats. The current research targets the key biomarkers that are sensitive to HS. In addition, the altered expression of genes related to HS response was detected by performing transcriptomic screening in blood, liver, and adrenal gland tissues post HS. Collectively...

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“…Bovine MECs (BMECs) in vitro culture are able to sense bacteria or bacterial products, and to react by upregulating the expression of several genes involved in the innate immune response (Chen et al 2014;Wang et al 2015). BMEC cultures were used as a model for udder tissue to profile the kinetics and extents of global changes in the transcriptome of BMEC after challenging them with heat-inactivated preparations of E. coli or S. aureus pathogens (Gunther et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Comparison of the effect of recombinant bovine wild and mutant lipopolysaccharide-binding protein in lipopolysaccharide-challenged bovine mammary epithelial cells

Sun

et al. 2016

Cell Stress and Chaperones

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Lipopolysaccharide (LPS)-binding protein (LBP) plays a crucial role in the recognition of bacterial components, such as LPS that causes an immune response. The aim of this study was to compare the different effects of recombinant bovine wild LBP and mutant LBP (67 Ala → Thr) on the LPSinduced inflammatory response of bovine mammary epithelial cells (BMECs). When BMECs were treated with various concentrations of recombinant bovine lipopolysaccharide-binding protein (RBLBP) (1, 5, 10, and 15 μg/mL) for 12 h, RBLBP of 5 μg/mL increased the apoptosis of BMECs induced by LPS without cytotoxicity, and mutant LBP resulted in a higher cell apoptosis than wild LBP did. By gene-chip microarray and bioinformatics, the data identified 2306 differentially expressed genes that were changed significantly between the LPSinduced inflamed BMECs treated with 5 μg/mL of mutant LBP and the BMECs only treated with 10 μg/mL of LPS (fold change ≥2). Meanwhile, 1585 genes were differently expressed between the inflamed BMECs treated with 5 μg/mL of wild LBP and 10 μg/mL of LPS-treated BMECs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed that these differentially expressed genes were involved in different pathways that regulate the inflammation response. It predicted that carriers of this mutation increase the risk for a more severe inflammatory response. Our study provides an overview of the gene expression profile between wild LBP and mutant LBP on the LPS-induced inflammatory response of BMECs, which will lead to further understanding of the potential effects of LBP mutations on bovine mammary glands.

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Effect of acute heat stress on adrenocorticotropic hormone, cortisol, interleukin-2, interleukin-12 and apoptosis gene expression in rats

Cited by 59 publications

References 25 publications

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Heat Stress Impairs the Physiological Responses and Regulates Genes Coding for Extracellular Exosomal Proteins in Rat

Comparison of the effect of recombinant bovine wild and mutant lipopolysaccharide-binding protein in lipopolysaccharide-challenged bovine mammary epithelial cells

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