4 research outputs found

    Adenosine Monophosphate-Activated Protein Kinase Signaling Regulates Lipid Metabolism in Response to Salinity Stress in the Red-Eared Slider Turtle Trachemys scripta elegans

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    Aquatic animals have developed various mechanisms to live in either hyperionic or hypoionic environments, and, as such, not many species are capable of surviving in both. The red-eared slider turtle, Trachemys scripta elegans, a well-known freshwater species, has recently been found to invade and inhabit brackish water. Herein, we focus on some of the metabolic adaptations that are required to survive and cope with salinity stress. The regulation of the adenosine monophosphate (AMP)-activated protein kinase (AMPK), a main cellular “energy sensor,” and its influence on lipid metabolism were evaluated with a comparison of three groups of turtles: controls in freshwater, and turtles held in water of either 5 salinity (S5) or 15 salinity (S15) with sampling at 6, 24, and 48 h and 30 days of exposure. When subjected to elevated salinities of 5 or 15, AMPK mRNA levels and AMPK enzyme activity increased strongly. In addition, the high expression of the peroxisome proliferator activated receptor-α (PPARα) transcription factor that, in turn, facilitated upregulation of target genes including carnitine palmitoyltransferase (CPT) and acyl-CoA oxidase (ACO). Furthermore, the expression of transcription factors involved in lipid synthesis such as the carbohydrate-responsive element-binding protein (ChREBP) and sterol regulatory element-binding protein 1c (SREBP-1c) was inhibited, and two of their target genes, acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), were significantly decreased. Moreover, exposure to saline environments also increased plasma triglyceride (TG) content. Interestingly, the content of low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) in plasma was markedly higher than the control in the S15 group after 30 days, which indicated that lipid metabolism was disrupted by chronic exposure to high salinity. These findings demonstrate that activation of AMPK might regulate lipid metabolism in r

    Antioxidant responses to salinity stress in an invasive species, the red-eared slider (Trachemys scripta elegans) and involvement of a TOR-Nrf2 signaling pathway

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    The red-eared slider (Trachemys scripta elegans), a freshwater turtle, is an invasive species in many parts of the world where it survives in both freshwater and coastal saline habitats. High salinity can induce reactive oxygen species (ROS) production and lead to oxidative damage. In this study, we investigate the antioxidant defense mechanisms of T. s. elegans in response to salinity stress. The results showed that the mRNA expression levels of superoxide dismutase (SODs), catalase (CAT) and glutathione peroxidase (GSH-PXs) were significantly increased in both 5 psu and 15 psu groups at the early stages of salinity exposure (generally 6–48 h), but typically returned to control levels after the longest 30 d exposure. In addition, hepatic and cardiac mRNA levels of the NF-E2-related factor 2 (Nrf2), showed a similar upregulation as an early response to stress, but decreased at 30 d in the 5 psu and 15 psu groups. The mRNA levels of the negative regulator of Nrf2, kelch-like ECH associating protein 1 (Keap1), exhibited the opposite pattern. Moreover, mRNA expression levels of target of rapamycin (TOR) and ribosomal protein S6 kinase 1 (S6K1) in liver and heart showed roughly similar patterns to those for Nrf2. Furthermore, the content of malondialdehyde (MDA) was significantly increased in liver, especially in the 15 psu group by ~2.5-fold. Taken together, these results indicate that T. s. elegans may activate the TOR-Nrf2 pathway to modulate antioxidant genes transcription in order to promote enhanced antioxidant defense in response to salinity stress

    Regulation of p53 in the red-eared slider (Trachemys scripta elegans) in response to salinity stress

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    The freshwater red-eared slider (Trachemys scripta elegans) is found not only in freshwater but also in coastal saline habitats. Hyperosmotic salinity can induce cell damage. p53, regarded as the guardian of the genome, is very important and versatile in response to the change of environment. In this study, the role of p53 in T. s. elegans under environmental salinity change will be explored. The results indicated that amino acid sequence of p53 showed high similarity to p53 of other species. In addition, the expression of p53 showed differences in various tissues under normal condition. Under salinity stress, the mRNA levels of p53 in the liver increased significantly at 48 h with 15‰ group (15 practical salinity units-exposed group). In the heart, p53 mRNA levels increased at 6 h in 5‰ (5 practical salinity units) and 15‰ groups. Furthermore, the changes of p21 mRNA expression levels in liver and heart were similar to p53, while cyclin D1, cyclin-dependent kinase4 (CDK4) and cyclin-dependent kinase6 (CDK6) showed opposite changes to p53. Moreover, Bax and caspase 3 mRNA expression levels were similar to p53, respectively, while Bcl-2 showed opposite changes. The positive cells of apoptosis were found in the liver of 15‰ at 48 h and 30 d of chronic stress. Taken together, these results indicated that the T. s. elegans may protect itself by regulating cell cycle progression and apoptosis of damaged cells under salinity stress, which played an important role for T. s. elegans in salinity adaptation

    Modulation of the intestinal barrier adaptive functions in red-eared slider (Trachemys scripta elegans) invading brackish waters

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    Globally, the increase in sea levels is leading to salinization of freshwater, which might influence the freshwater organisms such as red-eared slider, Trachemys scripta elegans. The turtle can invade brackish water environments, in which it must deal with elevated salinity in the gastrointestinal tract that could impact the intestinal function. The intestinal barrier provides a front-line of organismal defense against the chemical and biological environmental insults. In this study, the adaptive functions of the intestinal barrier including intestinal histomorphology, genes involved in intestinal barrier functions, and the intestinal micro-ecosystem were analyzed in the turtles exposed to freshwater (S0), 5‰ salinity (S5) and 15‰ salinity (S15) water for 30 days. The results showed that the intestine of T. s. elegans maintained normal histomorphological structure in the S5 group, whereas the villus height, crypt depth and the number of goblet cells in the S15 group were lower than that in the S5 and S0 groups. In addition, the relative expression levels of epithelial tight junction-related genes and intestinal immune-related genes in the gut were significantly upregulated in the S15 group, compared to the freshwater group. Mucin-2 gene expression was downregulated, but mucin-1 transcript levels were upregulated in salinity-treated groups. Furthermore, the abundances of phylum Proteobacteria, and genera Morganella and Aeromonas in the intestine were particularly enhanced in the S15 group than the S0 and S5 groups. Taken together, these results indicate that the intestinal barrier plays a protective role in T. s. elegans adaptation to brackish water environments. Our results provide a perspective on the evolution of salinity tolerance and help to evaluate the potential danger of the turtle to other species, and understand the challenges that other species must meet with rising sea levels
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