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PROVIDER: PRJNA1182409 | ENA |
REPOSITORIES: ENA
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Project description:Comparative Transcriptome Analysis of gonads in male and female Pseudobagrus ussuriensis (Bagridae, Siluriformes)
| PRJNA610419 | ENA
Project description:Saline is a key environmental parameter in aquaculture. Research on acute salinity stress can help farmers determine the optimal salinity level to reduce stress responses in fish larvae, improve survival rates, and increase production efficiencies. It can also aid in the selection or breeding of species suited to environments with specific salinities. However, the molecular mechanisms underlying the negative effects of high salinity on Pseudobagras ussuriensis and the regulatory mechanisms underlying its tolerance remain unclear. In this study, Pseudobagras ussuriensis was exposed to 10 g/L NaCl for 96 h, and the physiological and biochemical changes in the gill and kidney tissues were continuously monitored. Transcriptomic and metabolomic analyses of the gill and kidney tissues were conducted at 24 h to elucidate the molecular adaptation mechanisms to salt stress. A total of 2,554 differentially expressed genes (DEGs) were identified in gill and 1,066 DEGs in the kidney tissue, respectively. Compared with the control group, 826 genes were upregulated and 1,728 were downregulated in the gill tissue under acute salinity stress at 24 h, whereas 508 genes were upregulated and 558 were downregulated in the kidney tissue. These DEGs were involved in oxidative stress, energy metabolism, ion transport, and immune responses. Metabolomic analysis showed that compared to the control group, 85 differential metabolites (DMs) were identified in the gill tissue, with 49 upregulated and 36 downregulated, whereas 433 DMs were identified in the kidney tissue, with 252 upregulated and 181 downregulated. Notably, the levels of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) in the kidney and phosphatidic acid (PA) and PC in the gills were significantly increased, while sphingomyelin (SM) decreased. Integrated analysis of metabolomics and transcriptomics through the KGML network map revealed the downregulation of ALDH, ALDH7A1, AOX, and HADHA in the gill, and ENPP1_3, CD203, L-glutamine (downregulated), and Succinic Acid (upregulated) in the kidney. This study combined metabolomics, transcriptomics, and physiological-biochemical analyses to provide new insights into the molecular mechanisms of oxidative stress, energy metabolism, and immune regulation in gill and kidney tissues under acute salinity stress.
2025-04-03 | GSE292974 | GEO
Project description:With the development of the poultry industry, ammonia, as a main contaminant in the air, is causing increasing problems with broiler health. To date, most studies of ammonia toxicity have focused on the nervous system and the gastrointestinal tract in mammals. However, few detailed studies have been conducted on the hepatic response to ammonia toxicity in poultry. The molecular mechanisms that underlie these effects remain unclear. In the present study, our group applied isobaric tags for relative and absolute quantitation (iTRAQ) - based quantitative proteomic analysis to investigate changes in the protein profile change in hepatic tissue of broilers exposed to high concentrations of atmospheric ammonia, with the goal of characterizing the molecular mechanisms of chronic liver injury from exposure to high ambient levels of ammonia. Overall, 30 differentially expressed proteins that are involved in nutrient metabolism (energy, lipid and amino acid), immune response, transcriptional and translational regulation, stress response and detoxification were identified. In particular, two of these proteins, beta-1 galactosidase (GLB1), and a kinase (PRKA) anchor protein 8-like (AKAP8 L), were previously suggested to be potential biomarkers of chronic liver injury. In addition to the changes in the protein profile, serum parameters and histochemical analyses of hepatic tissue also showed extensive hepatic damage in ammonia-exposed broilers. Altogether, these findings suggest that longtime exposure to high concentrations of atmospheric ammonia can trigger chronic hepatic injury in broilers via different mechanisms, providing new information that can be used for intervention using nutritional strategies in the future.
2016-06-15 | PXD001670 | Pride
Project description:Abstract: Atmospheric ammonia is a common problem in poultry industry. High concentrations of aerial ammonia cause great harm to broilers' health and production. For the consideration of human health, the limit exposure concentration of ammonia in houses is set at 25 ppm. Previous reports have shown that 25 ppm is still detrimental to livestock, especially the gastrointestinal tract and respiratory tract, but the negative relationship between ammonia exposure and the tissue of breast muscle of broilers is still unknown. In the present study, 25 ppm ammonia in poultry houses was found to lower slaughter performance and breast yield. Then, high-throughput RNA sequencing was utilized to identify differentially expressed genes in breast muscle of broiler chickens exposed to high (25 ppm) or low (3 ppm) levels of atmospheric ammonia. The transcriptome analysis showed that 163 genes (fold change ≥ 2 or ≤ 0.5; P-value < 0.05) were differentially expressed between Ammonia25 (treatment group) and Ammonia3 (control group), including 96 down-regulated and 67 up-regulated genes. qRT-PCR analysis validated the transcriptomic results of RNA sequencing. Gene Ontology (GO) functional annotation analysis revealed potential genes, processes and pathways with putative involvement in growth and development inhibition of breast muscle in broilers caused by aerial ammonia exposure. This study facilitates understanding of the genetic architecture of the chicken breast muscle transcriptome, and has identified candidate genes for breast muscle response to atmospheric ammonia exposure.
2016-08-19 | GSE85786 | GEO
Project description:The liver is the largest detoxification organ in the human body. RNA sequencing (RNA-seq) analyses of liver samples were performed to investigate the effects of high ammonia levels (ammonia exposure at 75 ± 5 ppm), a low ammonia level (ammonia exposure at 5 ± 5 ppm) was set as control group, on the metabolism and detoxification capabilities of laying ducks.
2020-02-08 | GSE144924 | GEO
Project description:Investigation of the whole genome gene expression level changes relative to exponential phase growth in Nitrosomonas europaea ATCC19718 after 12 hours ammonia starvation, 144 hours ammonia starvation, and 20 minutes following ammonia addition to starved cells. The ammonia monooxygenase of chemolithotrophic ammonia oxidizing bacteria (AOB) catalyzes the first step in ammonia oxidation by converting ammonia to hydroxylamine. The monooxygenase of Nitrosomonas europaea is encoded by two nearly identical operon copies (amoCAB1,2). Several AOB, including N. europaea, also posess a divergent monocistronic copy of amoC (amoC3) of unknown function. Previous work suggested a possible functional role for amoC3 in N. europaea during recovery from extended ammonia starvation as part of the σE- stress response regulon during the recovery of N. europaea from extended ammonia starvation, thus indicating its importance during the exit of cells from starvation. We here used global transcription analysis to show that expression of amoC3 is part of a general post-starvation cellular response system in N. europaea. We also found that amoC3 is required for efficient exit from prolonged ammonia starvation, as deleting this gene impaired growth at elevated temperatures and recovery following starvation under high oxygen tensions. Deletion of the σ32 global stress response regulator demonstrated that the heat shock regulon also plays a significant role in mediating the recovery of N. europaea from starvation. These findings provide the first described phenotype associated with the divergent AmoC3 subunit which appears to function as a stress responsive subunit capable of maintaining ammonia oxidation activity under stress conditions.
2012-08-03 | GSE35122 | GEO
Project description:To gain insight into the molecular mechanism of PuHox52-mediated low-N adaption, we performed a transcriptome sequencing analysis (RNA-seq) using the PuHox52-OE lines and WT P. ussuriensis in roots under low-N for 3 wks, as well as roots under normal-N as controls.
2025-04-02 | GSE200009 | GEO
Project description:The liver is frequently challenged by surgery-induced metabolic overload, viruses, or toxins, which induce the formation of reactive oxygen species. To determine the effect of oxidative stress on liver regeneration and to identify the underlying signalling pathways, we studied liver repair in mice lacking the Nrf2 transcription factor. In these animals, expression of several cytoprotective enzymes was reduced in hepatocytes, resulting in oxidative stress. As a consequence, tissue damage was aggravated, and liver regeneration after partial hepatectomy was delayed. Using in vitro and in vivo studies we identified oxidative stress-induced insulin/insulin-like growth factor resistance as the underlying mechanism. This deficiency impaired the activation of p38 mitogen-activated kinase, Akt kinase, and downstream targets after hepatectomy, resulting in enhanced death and delayed proliferation of hepatocytes. Our results reveal novel roles of Nrf2 in the regulation of growth factor signalling and in tissue repair. In addition, they provide new insight into the mechanisms underlying oxidative stress-induced defects in liver regeneration and thus offer new avenues to improve regeneration in patients with acute or chronic liver damage. Experiment Overall Design: Livers from Nrf2 k.o. and wt mice; 3 hybridizations per genoype: RNA samples were pooled from 3 individual animals
2008-06-16 | E-GEOD-8969 | biostudies-arrayexpress