Ontology highlight
ABSTRACT:
PROVIDER: PRJNA991337 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25194533.fastq.gz | Fastqsanger.gz | |||
| SRR25194534.fastq.gz | Fastqsanger.gz | |||
| SRR25194535.fastq.gz | Fastqsanger.gz | |||
| SRR25194536.fastq.gz | Fastqsanger.gz | |||
| SRR25194537.fastq.gz | Fastqsanger.gz |
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Project description:Heat illness, which remains an occupational and environmental hazard, can be caused by excessive strain or heat load in combination with other factors. In the 10-year period from 1999 to 2009, an average of 658 annual heat-related deaths occurred in the United States. While heat stress at the cellular level has been studied, a paucity of risk assessment and injury biomarkers as well as therapeutic interventions remains. To identify novel biomarkers and to further understand the molecular mechanisms of heat stress, we identified differentially expressed microRNAs (miRNAs) in the heart, liver, and kidney from a conscious rat model at three time points. We distinguished the effect in animals with histopathological evidence of heart injury from those without evidence of organ injury. In animals without evidence of injury, we identified a total of 45 unique modulated miRNAs, whereas in the three animals with evidence of injury, we identified 171 unique differentially expressed miRNAs. The majority of the perturbed miRNAs were both time and tissue specific. Using the data from a microarray companion study, we identified the mRNAs that are the predicted targets of the differentially expressed miRNAs and performed pathway enrichment analysis. The enrichment analysis suggested that the perturbed miRNAs are involved in biological pathways related to energy metabolism, the unfolded protein response, and organ injury. These miRNAs may serve as organ-specific heat stress biomarkers of exposure or effect, as well as identify potential targets of heat illness prevention.
2016-08-10 | GSE81331 | GEO
Project description:Heat illness, which remains an occupational and environmental hazard, can be caused by excessive strain or heat load in combination with other factors. In the 10-year period from 1999 to 2009, an average of 658 annual heat-related deaths occurred in the United States. While heat stress at the cellular level has been studied, a paucity of risk assessment and injury biomarkers as well as therapeutic interventions remains. To identify novel biomarkers and to further understand the molecular mechanisms of heat stress, we identified differentially expressed microRNAs (miRNAs) in the heart, liver, and kidney from a conscious rat model at three time points. We distinguished the effect in animals with histopathological evidence of heart injury from those without evidence of organ injury. In animals without evidence of injury, we identified a total of 45 unique modulated miRNAs, whereas in the three animals with evidence of injury, we identified 171 unique differentially expressed miRNAs. The majority of the perturbed miRNAs were both time and tissue specific. Using the data from a microarray companion study, we identified the mRNAs that are the predicted targets of the differentially expressed miRNAs and performed pathway enrichment analysis. The enrichment analysis suggested that the perturbed miRNAs are involved in biological pathways related to energy metabolism, the unfolded protein response, and organ injury. These miRNAs may serve as organ-specific heat stress biomarkers of exposure or effect, as well as identify potential targets of heat illness prevention. Heart, liver, lung and kidney tissue was collected from rats at Tc,max and at 24 and 48 h for both heat exposed rats (n=4 to 6) or time matched, unheated controls (n= 4 to 6)
2016-08-10 | E-GEOD-81331 | biostudies-arrayexpress
Project description:Prolonged exposure to high temperatures may cause heat-related illnesses, such as cramps, syncope, exhaustion or even stroke in some individuals. Heat-related injuries remain a threat to the health and operational effectiveness of military personnel, athletes and the general public. Heat injury victims experience long-term complications that may include multi-system organ (liver, kidney, muscle) and neurologic damage, as well as reduced exercise capacity and heat intolerance. Findings from our laboratory using a developed heat stress model show that about 1/3 of mice are heat-intolerant and vulnerable to heat injury even though they are from the same mice litter. We examined if there is any genetic causation to this pattern of observation between the two groups of mice classified (Heat Intolerant and Heat Tolerant). We would like to screen Heat Tolerant and Heat Intolerant mice samples using microarray technology and examine their microRNA and mRNA for possible gene-specific differences between the two groups (6 mice per group). The results from this proposed animal research will help identify and select potential markers that can be used as a pre-screen to identify heat intolerance and assess heat injury recovery in humans.
2013-09-01 | GSE48270 | GEO
Project description:Heat stress exposure in intermittent heat waves and subsequent exposure during war theaters is a clinical challenge that can lead to multi-organ dysfunction and long-term complications in the elderly. Using an aged mouse model and high-throughput sequencing, this study investigated the molecular dynamics of the liver-brain connection during heat stress exposure. Distinctive gene expression patterns induced by periodic heat stress emerged in both brain and liver tissues. An altered transciptome showed heat stress-induced altered acute phase response pathways, causing neural, hepatic, and systemic inflammation, and impaired synaptic plasticity. Results also showed that proinflammatory molecules S100B, IL-17, IL-33 and neurological disease signaling pathways were upregulated, while protective pathways like aryl hydrocarbon receptor signaling were downregulated. In parallel, Rantes, IRF7, NOD1/2, TREM1, and hepatic injury signaling pathways were upregulated.
2024-05-15 | GSE252887 | GEO
Project description:Prolonged exposure to high temperatures may cause heat-related illnesses, such as cramps, syncope, exhaustion or even stroke in some individuals. Heat-related injuries remain a threat to the health and operational effectiveness of military personnel, athletes and the general public. Heat injury victims experience long-term complications that may include multi-system organ (liver, kidney, muscle) and neurologic damage, as well as reduced exercise capacity and heat intolerance. Findings from our laboratory using a developed heat stress model show that about 1/3 of mice are heat-intolerant and vulnerable to heat injury even though they are from the same mice litter. We examined if there is any genetic causation to this pattern of observation between the two groups of mice classified (Heat Intolerant and Heat Tolerant). We would like to screen Heat Tolerant and Heat Intolerant mice samples using microarray technology and examine their microRNA and mRNA for possible gene-specific differences between the two groups (6 mice per group). The results from this proposed animal research will help identify and select potential markers that can be used as a pre-screen to identify heat intolerance and assess heat injury recovery in humans. Heat-induced physiological and biochemical changes were assessed to determine heat tolerance levels in mice. We performed mRNA and microRNA expression profiling on mouse gastrocnemius muscle tissue samples to determine novel biological pathways associated with heat tolerance.
2013-09-01 | E-GEOD-48269 | biostudies-arrayexpress
Project description:Prolonged exposure to high temperatures may cause heat-related illnesses, such as cramps, syncope, exhaustion or even stroke in some individuals. Heat-related injuries remain a threat to the health and operational effectiveness of military personnel, athletes and the general public. Heat injury victims experience long-term complications that may include multi-system organ (liver, kidney, muscle) and neurologic damage, as well as reduced exercise capacity and heat intolerance. Findings from our laboratory using a developed heat stress model show that about 1/3 of mice are heat-intolerant and vulnerable to heat injury even though they are from the same mice litter. We examined if there is any genetic causation to this pattern of observation between the two groups of mice classified (Heat Intolerant and Heat Tolerant). We would like to screen Heat Tolerant and Heat Intolerant mice samples using microarray technology and examine their microRNA and mRNA for possible gene-specific differences between the two groups (6 mice per group). The results from this proposed animal research will help identify and select potential markers that can be used as a pre-screen to identify heat intolerance and assess heat injury recovery in humans. Heat-induced physiological and biochemical changes were assessed to determine heat tolerance levels in mice. We performed mRNA and microRNA expression profiling on mouse gastrocnemius muscle tissue samples to determine novel biological pathways associated with heat tolerance.
2013-09-01 | E-GEOD-48270 | biostudies-arrayexpress
Project description:Prolonged exposure to high temperatures may cause heat-related illnesses, such as cramps, syncope, exhaustion or even stroke in some individuals. Heat-related injuries remain a threat to the health and operational effectiveness of military personnel, athletes and the general public. Heat injury victims experience long-term complications that may include multi-system organ (liver, kidney, muscle) and neurologic damage, as well as reduced exercise capacity and heat intolerance. Findings from our laboratory using a developed heat stress model show that about 1/3 of mice are heat-intolerant and vulnerable to heat injury even though they are from the same mice litter. We examined if there is any genetic causation to this pattern of observation between the two groups of mice classified (Heat Intolerant and Heat Tolerant). We would like to screen Heat Tolerant and Heat Intolerant mice samples using microarray technology and examine their microRNA and mRNA for possible gene-specific differences between the two groups (6 mice per group). The results from this proposed animal research will help identify and select potential markers that can be used as a pre-screen to identify heat intolerance and assess heat injury recovery in humans.
2013-09-01 | GSE48269 | GEO
Project description:Rainbow trout is a typical cold-water fish, with the intensification of global warming, high temperatures severely restrict the development of aquaculture in summer. Understanding the molecular regulation mechanisms of rainbow trout in response to heat stress will be salutary to alleviate heat stress-related damage. In the present study, we performed transcriptome analysis of liver tissues in rainbow trout under heat stress (24℃) and control (18℃) conditions to identify induced lncRNAs and pathways by heat stress. More than 658 million clean reads and 5,916 lncRNAs were identified from six liver libraries. A total of 927 novel lncRNAs were generated and 428 differentially expressed lncRNAs were screened through stringent thresholds. The RNA-seq results were verified by RT-qPCR. In addition, the regulatory network of important functional lncRNA-mRNA were constructed. GO and KEGG enrichment analysis of target gene of differentially expressed lncRNAs were performed. Many target genes involved in maintaining homeostasis or adapting to stress and stimuli were highly induced under heat stress. Several important regulatory pathways were involved in heat stress, including thyroid hormone signaling pathway, PI3K-Akt signaling pathway, estrogen signaling pathway, etc. This result broadens our understanding of lncRNA associated with heat stress and provides new insights into lncRNA-mediated regulation of rainbow trout heat stress.
2019-08-11 | GSE135668 | GEO
Project description:Trained immunity is classically characterized by long-term epigenetic reprogramming of innate immune cells to combat infectious diseases. Infection-induced organ injury is a common clinical severity phenotype of sepsis. However, whether the induction of trained immunity plays a role in protecting septic-organ injury remains largely unknown. Here, through establishing an in vivo β-glucan training and secondary LPS challenge-induced organ injury model in zebrafish larvae, we observe that induction of trained immunity could inhibit the pyroptosis of hepatocytes to alleviate septic-liver injury, with an elevated epigenetic modification of trimethylation at histone 3 lysine 4 (H3K4me3) that targets mitophagy activation. Moreover, we identify a novel C-type lectin domain receptor in zebrafish, named DrDectin-1, which is revealed as the orchestrator in gating H3K4me3 rewiring-mediated mitophagy activation and alleviating the pyroptosis-engaged septic-liver injury in vivo. Taken together, our results uncover a tissue-resident trained immunity in maintaining tissue homeostasis at a whole animal level, and offer a facile in vivo model to efficiently integrate trained immunity for immunotherapies.
2024-04-25 | GSE245156 | GEO