Proteomic profiling of heat illness pateiens
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Jingchun Song
PROVIDER: PXD064588 | iProX | Tue Jun 03 00:00:00 BST 2025
REPOSITORIES: iProX
Publications
Developing a molecular diagnostic model for heatstroke-induced coagulopathy: a proteomics and metabolomics approach.
Zeng Qingbo Q Lin Qingwei Q He Longping L Zhong Lincui L Zhou Ye Y Deng Xingping X Zhang Nianqing N Song Qing Q Song Jingchun J
Frontiers in molecular biosciences 20250620
<h4>Background</h4>Heatstroke (HS) is becoming more concerning, with coagulopathy contributing to higher mortality. The aim of this study was to analyze the metabolomic and proteomic profiles associated with heatstroke-induced coagulopathy (HSIC) and to develop a molecular diagnostic model based on proteomic and metabolomic patterns.<h4>Methods</h4>This study included 41 HS patients from the Department of Critical Care Medicine at a comprehensive teaching hospital. Plasma proteins and metabolite ...[more]
Similar Datasets
Project description:No ideal serum biomarker currently exists for the early diagnosis of colorectal cancer (CRC). Therefore, it is urgent that accurate and reliable serum biomarkers be identified.
| 2125831 | ecrin-mdr-crc
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:Background: The in vivo gene response associated with hyperthermia and subsequent return to homeostasis or development of heat illness is poorly understood. Early activation of gene networks in the heat stress response is likely to lead to the systemic inflammation, multi-organ functional impairment, and other pathophysiological states characteristic of heat illness. Here, we perform an unbiased global characterization of the multi-organ gene response using an in vivo model of heat stress in the conscious rat. Results: Rats were subjected to elevated temperatures until implanted thermal probes indicated a maximal core temperature of 41.8 °C (Tc,Max). Liver, lung, kidney, and heart were harvested at Tc,Max, 24 hours, and 48 hours after heat stress in groups of experimental animals and time-matched controls kept at ambient temperature. Clinical chemistries suggested abnormal function in liver, kidney, and lung at Tc,Max, and cardiac histopathology at 48 hours supported persistent cardiac damage in 3 out of 6 animals. Microarray analysis identified 78 differentially expressed genes common to all 4 organs at Tc,Max (i.e., the consensus heat stress response). Gene set enrichment analysis of gene ontology terms identified 25 biological processes in 4 general gene ontology categories: protein folding, regulation of apoptosis, response to cytokines, and transcriptional responses. Functional analysis clustering of the 78 differentially expressed genes in the consensus heat stress response also identified functional categories of protein folding and regulation of apoptosis. Self-organizing maps identified gene-specific signatures corresponding to protein folding disorders specific to only heat-stressed rats with histopathologic evidence of cardiac injury at 48 hours. Enrichment analysis of differentially expressed proteins in heat-injured hearts at 48 hours corroborated gene enrichment analysis results. Quantitative proteomics analysis by iTRAQ demonstrated that differential protein expression was not comparable to transcript expression at Tc,Max and 24 hours. However, the profile of differentially expressed proteins closely matched the transcriptomic profile in heat-injured animals at 48 hours. Pathway analysis at both the transcript and protein levels supported catastrophic deficits in energetics and cellular metabolism, chronic proteotoxic response, and activation of the unfolded protein response. Calculation of protein super-saturation scores demonstrated an increased propensity of proteins to aggregate in the hearts of heat-injured animals at 48 hours, consistent with accumulation of misfolded proteins. Conclusions: Global transcriptomic and proteomic analysis identified networks of genes and proteins initiating an unfolded protein response, metabolic dysfunction, and mitochondrial energy crisis in animals with histopathologic evidence of persistent heat injury, providing the basis for a systems-level physiological model of heat illness and recovery.
2015-01-14 | GSE56740 | GEO
Project description:Salmonella Heidelberg is currently the 9th common serovar and has more than twice the average incidence of blood infections in Salmonella. A recent Salmonella Heidelberg outbreak in chicken infected 634 people during 2013-2014, with a hospitalization rate of 38% and an invasive illness rate of 15%. While the company’s history suggested longstanding sanitation issues, the strains’ characteristics which may have contributed to the outbreak are unknown. We hypothesized that the outbreak strains of S. Heidelberg might possess enhanced stress tolerance or virulence capabilities. Consequently, we obtained nine food isolates collected during the outbreak investigation and several reference isolates and tested their tolerance to processing stresses, their ability to form biofilms, and their invasiveness in vitro. We further performed RNA-sequencing on three isolates with varying heat tolerance to determine the mechanism behind our isolates’ enhanced heat tolerance. Ultimately, we determined that (i) many Salmonella Heidelberg isolates associated with a foodborne outbreak have enhanced heat resistance (ii) Salmonella Heidelberg outbreak isolates have enhanced biofilm-forming ability under stressful conditions, compared to the reference strain (iii) exposure to heat stress may also increase Salmonella Heidelberg isolates’ antibiotic resistance and virulence capabilities and (iv) Salmonella Heidelberg outbreak-associated isolates are primed to better survive stress and cause illness. This data helps explain the severity and scope of the outbreak these isolates are associated with and can be used to inform regulatory decisions on Salmonella in poultry and to develop assays to screen isolates for stress tolerance and likelihood of causing severe illness.
2018-09-01 | GSE103418 | GEO
Project description:These experiments aim to detect changes in the transcript (mRNA) of cardiac tissue when animals are exposed to high temperatures and heat stroke occurs due to the increase in environmental temperature. The research objectives include: 1) detecting changes in transcripts (mRNA) of heart tissue during heat stroke caused by elevated environmental temperatures; 2) Detecting transcripts that can serve as biomarkers for heat stroke induced myocardial injury.
2025-07-26 | GSE303366 | GEO
Project description:Background: The in vivo gene response associated with hyperthermia and subsequent return to homeostasis or development of heat illness is poorly understood. Early activation of gene networks in the heat stress response is likely to lead to the systemic inflammation, multi-organ functional impairment, and other pathophysiological states characteristic of heat illness. Here, we perform an unbiased global characterization of the multi-organ gene response using an in vivo model of heat stress in the conscious rat. Results: Rats were subjected to elevated temperatures until implanted thermal probes indicated a maximal core temperature of 41.8 M-BM-0C (Tc,Max). Liver, lung, kidney, and heart were harvested at Tc,Max, 24 hours, and 48 hours after heat stress in groups of experimental animals and time-matched controls kept at ambient temperature. Clinical chemistries suggested abnormal function in liver, kidney, and lung at Tc,Max, and cardiac histopathology at 48 hours supported persistent cardiac damage in 3 out of 6 animals. Microarray analysis identified 78 differentially expressed genes common to all 4 organs at Tc,Max (i.e., the consensus heat stress response). Gene set enrichment analysis of gene ontology terms identified 25 biological processes in 4 general gene ontology categories: protein folding, regulation of apoptosis, response to cytokines, and transcriptional responses. Functional analysis clustering of the 78 differentially expressed genes in the consensus heat stress response also identified functional categories of protein folding and regulation of apoptosis. Self-organizing maps identified gene-specific signatures corresponding to protein folding disorders specific to only heat-stressed rats with histopathologic evidence of cardiac injury at 48 hours. Enrichment analysis of differentially expressed proteins in heat-injured hearts at 48 hours corroborated gene enrichment analysis results. Quantitative proteomics analysis by iTRAQ demonstrated that differential protein expression was not comparable to transcript expression at Tc,Max and 24 hours. However, the profile of differentially expressed proteins closely matched the transcriptomic profile in heat-injured animals at 48 hours. Pathway analysis at both the transcript and protein levels supported catastrophic deficits in energetics and cellular metabolism, chronic proteotoxic response, and activation of the unfolded protein response. Calculation of protein super-saturation scores demonstrated an increased propensity of proteins to aggregate in the hearts of heat-injured animals at 48 hours, consistent with accumulation of misfolded proteins. Conclusions: Global transcriptomic and proteomic analysis identified networks of genes and proteins initiating an unfolded protein response, metabolic dysfunction, and mitochondrial energy crisis in animals with histopathologic evidence of persistent heat injury, providing the basis for a systems-level physiological model of heat illness and recovery. To induce the pathophysiological effects of heat stress, conscious rats were placed in an incubator at 37M-BM-:C and their core temperature was monitored. Animals were sacrificed when their core temperature reached 41.8M-BM-:C (Tc,Max), or they were returned to their normal housing environment and were allowed to recover for up to 24 or 48 hours prior to sacrifice. Time-matched controls were euthanized at times corresponding to Tc,Max, 24 hours, and 48 hours. For each condition n=6 for a total of 36 animals. Four tissues (liver, lung, kidney and heart) were analyzed from each animal for a total of 144 arrays; however a few arrays did not pass QC therefore only 140 are reported here: 34 liver, 35 lung, 36 kidney, or 35 heart.
2015-01-14 | E-GEOD-56740 | biostudies-arrayexpress
Project description:Spinach (Spinacia oleracea L.) is an economically important and globally consumed popular leafy vegetable that is heat-sensitive. Heat stress caused by global climate change is one of the primary deleterious elements limiting spinach production worldwide. Little work has been done to explore the heat-responsive mechanisms of spinach under high temperature-induced stress. In the present study, we used iTRAQ-based proteomic and transcriptomic approaches to investigate physiological, metabolic, and proteomic responses of spinach in response to day / night temperature of 35°C / 25°C compared to 20°C / 15°C for 4 days. A total of 3,543 differentially expressed genes (DEGs) were detected using transcriptome sequencing, of which 2,086 DEGs were downregulated and 1,457 were upregulated. The DEGs were mainly involved in superoxide dismutase activity, catalase, and peroxidase activity. A total of 3,246 differentially abundant proteins were detected using iTAQ-based quantitative proteomic approach, from which 567 differentially expressed proteins (DEPs) (277 upregulated and 290 downregulated) were identified. DEPs were mainly assigned to pathways related to metabolism, signal transduction, protein degradation, defense, and antioxidant. Four genes - superoxide dismutase (SOD, LOC110788339), catalase (CAT, LOC110790286), peroxidase (POD, LOC110775253), and heat shock protein (HSP, LOC110799288) - were validated using quantitative real-time PCR (qRT-PCR) to verify the proteomic and transcriptomic analyses, showing different transcriptional and translational expression levels. The findings of this study provide a fundamental understanding of the metabolic pathways and biological processes that control adaptation to heat stress in spinach, and provide novel insight into the development of heat-tolerant spinach.
2020-06-24 | GSE153070 | GEO
Project description:Yeast Saccharomyces cerevisiae has been widely used as a model system for studying genomic instability. In this study, heat-shock-induced genomic alterations were explored in the heterozygous diploid yeast strain JSC25-1. In combination of the whole-genome microarray, the patterns of chromosomal instability induced by heat shock could also be explored at a whole genome level. Using this system, we found heat-shock treatment resulted in hundreds-fold higher rate of genomic alterations, including aneuploidy and loss of heterozygosity (LOH).
2020-05-18 | GSE150711 | GEO
Project description:Jujube (Ziziphus jujuba Mill.) is an economically and agriculturally significant fruit crop and is widely cultivated throughout the world. Heat stress has recently become one of the major abiotic stresses limiting plant growth and productivity. However, there are few studies on the transcriptome profiling of jujube subjected to heat stress. In this study, we analyzed the physiological and transcriptomic changes of heat-resistant jujube cultivar ‘HR’ and heat-sensitive cultivar ‘HS’ caused by high temperature stress. We statistically determined 984, 1468, 1727 and 2098 differentially expressed genes (DEGs) between ‘HR’ and ‘HS’ after 0, 1, 3, 5 d of heat stress, respectively. Gene Ontology (GO) enrichment analysis indicated that Aa great deal of heat-responsive genes were identified in these DEGs by Gene Ontology (GO) enrichment analysis. It suggests the distinct molecular mechanism of jujube response to heat stress. Furthermore, we validated the expression profiles of 12 candidates using qRT-PCR to further confirm the accuracy of the RNA-seq data. These results will advance our knowledge of the genes involved in the complex regulatory networks of heat stress and provide genetic resources for further improving the heat tolerance in jujube.
2020-10-02 | GSE136383 | GEO