Transcriptomic changes in Arabidopsis thaliana seedlings in response to traffic noise exposure
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1005259 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25634647.fastq.gz | Fastqsanger.gz | |||
| SRR25634648.fastq.gz | Fastqsanger.gz | |||
| SRR25634649.fastq.gz | Fastqsanger.gz | |||
| SRR25634650.fastq.gz | Fastqsanger.gz | |||
| SRR25634651.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Seeds in the experimental group were exposed to 48 h of traffic noise recorded in a highly congested area of the city, while the control group was kept under background white noise. While traffic noise exposure made no effects on seed germination, noise treatment significantly increased the growth of seedlings by 39%. By employing RNA-sequencing profiling, we further investigated the noise-induced molecular changes in the A. thaliana seedlings. The aberrant expression of 690 genes was detected in the noise-exposed seedlings.
2023-10-15 | GSE240794 | GEO
Project description:Environmental stressors present in the modern world can have a fundamental effect on the physiology and health of humans. Exposure to stressors like air pollution, heat and traffic noise has been linked to a pronounced increase in non-communicable diseases. Specifically, aircraft noise has been identified as a risk factor for cardiovascular and metabolic diseases, such as arteriosclerosis, heart failure, stroke and diabetes. Noise stress leads to neuronal activation with subsequent stress hormone release that ultimately leads to activation of the renin-angiotensin-aldosterone system, increasing inflammation and oxidative stress, with dramatic effects on the cardiovascular system. However, despite the epidemiological evidence of a link between noise stress and metabolic dysfunction, the consequences of exposure at the molecular, metabolic level of the cardiovascular system are largely unknown. Here we use a murine model system of aircraft noise exposure to show that noise stress profoundly alters heart metabolism. Within days of exposing animals to aircraft noise the heart has a reduced potential for utilising fatty-acid beta-oxidation, the tricarboxylic acid cycle, and the electron transport chain for generating ATP. This is compensated by shifting energy production towards glycolysis. Intriguingly, the metabolic shift is reminiscent of what is observed in failing and ischaemic hearts. Our results demonstrate that within a relatively short exposure time, the cardiovascular system undergoes a fundamental metabolic shift that bears the hallmarks of cardiovascular disease. Overall, aircraft noise induces rapid, detrimental metabolic shifts in the heart, resembling patterns seen in cardiovascular diseases. These findings underscore the urgent need to comprehend molecular consequences of environmental stressors, paving the way for targeted interventions aiming mitigating health risks associated with chronic noise exposure in our modern, noisy environments.
2025-05-14 | PXD051406 | Pride
Project description:The molecular mechanisms underlying the great differences in susceptibility to noise-induced hearing loss (NIHL) exhibited by both humans and laboratory animals are unknown. Using microarray technology, the present study demonstrates that the effects of noise overexposure on the expression of molecules likely to be important to the development of NIHL differ among inbred mice that have distinctive susceptibilities to NIHL including B6.CAST, 129X1/SvJ, and 129S1/SvImJ. The noise-exposure protocol produced, on average, a permanent loss of about 40 dB in sensitivity for auditory brainstem responses in susceptible B6.CAST mice, but no threshold elevations for the two resistant 129S1/SvImJ and 129X1/SvJ substrains. Measurements of noise-induced gene expression changes 6 h after the noise exposure revealed significant alterations in the expression levels of 48 genes in the resistant mice, while by these same criteria, there were seven differentially expressed genes in the susceptible B6.CAST mice. Differentially expressed genes in both groups of mice included subsets of transcription factors. However, only in the resistant mice was there a significant induction of proteins involved in cell-survival pathways such as HSP70, HSP40, p21, GADD45ï¢, Ier3, and Nfï«ï¢iïº. Moreover, increased expression of three of these factors after noise was confirmed at the protein level. Drastically enhanced HSP70, GADD45ï¢, and p21 immunostaining were detected 6 h after the noise exposure in subsets of cells of the lateral wall, spiral limbus, and organ of Corti as well as in cochlear nerve fibers. Upregulation of these proteins after noise exposure likely contributes to the prevalence of survival cellular pathways and thus to the resistance to NIHL that is characteristic of the 129X1/SvJ mice. Experiment Overall Design: Female 10-wk-old mice of the B6.CAST and 129X1/SvJ strains were divided randomly into non-noise control and noise-exposure groups. The non-noise mice served as controls in the gene-profiling experiments to control for the stress induced by experimenter handling and/or confinement of the mice in the noise-exposure chamber that was not directly related to the noise. This mice were in the noise chamber for a sham exposure. In contrast, the ânoiseâ groups were exposed to a 105-dB SPL, 10-kHz octave band of noise for 1 h and sacrificed 6 h after the exposure. Of each of these major groups, eight mice were used for each of three 129X1/SvJ control and three noise-exposed 129X1/SvJ arrays and two B6.CAST control and two noise-exposed B6.CAST arrays. Consequently within each subgroup the arrays are biological replicates.
2008-10-25 | E-GEOD-8342 | biostudies-arrayexpress
Project description:Traffic-related air pollution has been a common public health problem, which is associated with central nervous system dysfunction according to large-scale epidemiological studies. Current studies are mostly limited to artificial laboratory exposure environments and specific genetic mechanisms remain unclear. In the spring, we transported the aged mice from the laboratory to the 1-meter-high dry platform in the campus and tunnel at the same time. Aged mice were exposed form 7 am to 7 pm each day for 2, 4 and 12 weeks, respectively. Compared with the control group (in campus), the memory function of mice in the exposure group (in tunnel) was significantly impaired in Morris water maze. Traffic-related air pollution exposure increased the number of activated microglia in the hippocampal DG and CA1, and up-regulated mRNA expression of inflammatory factors IL-18, IL-1β, IL-6 and TNF-α. By screening the risk genes of Alzheimer’s disease, we found the mRNA and protein levels of ABCA7 were down-regulated and those of PYK2 were up-regulated in the dorsolateral prefrontal cortex (dPFC) of aged mice. The DNA methylation ratio increased in four CpG sites of abca7 promoter region and decreased in one CpG site of pyk2 promoter region, which were consistent with the altered expression of ABCA7 and PYK2. In conclusion, exposure to the real traffic environment impaired memory function and enhanced neuroinflammation of aged mice, which could be relevant to the alteration of ABCA7 and PYK2 gene expression. Our work provided a new and promising understanding of the pathological mechanisms of cognitive impairment caused by traffic-related air pollution.
2022-07-16 | GSE208109 | GEO
Project description:The molecular mechanisms underlying the great differences in susceptibility to noise-induced hearing loss (NIHL) exhibited by both humans and laboratory animals are unknown. Using microarray technology, the present study demonstrates that the effects of noise overexposure on the expression of molecules likely to be important to the development of NIHL differ among inbred mice that have distinctive susceptibilities to NIHL including B6.CAST, 129X1/SvJ, and 129S1/SvImJ. The noise-exposure protocol produced, on average, a permanent loss of about 40 dB in sensitivity for auditory brainstem responses in susceptible B6.CAST mice, but no threshold elevations for the two resistant 129S1/SvImJ and 129X1/SvJ substrains. Measurements of noise-induced gene expression changes 6 h after the noise exposure revealed significant alterations in the expression levels of 48 genes in the resistant mice, while by these same criteria, there were seven differentially expressed genes in the susceptible B6.CAST mice. Differentially expressed genes in both groups of mice included subsets of transcription factors. However, only in the resistant mice was there a significant induction of proteins involved in cell-survival pathways such as HSP70, HSP40, p21, GADD45beta, Ier3, and Nf-kappaB. Moreover, increased expression of three of these factors after noise was confirmed at the protein level. Drastically enhanced HSP70, GADD45beta, and p21 immunostaining were detected 6 h after the noise exposure in subsets of cells of the lateral wall, spiral limbus, and organ of Corti as well as in cochlear nerve fibers. Upregulation of these proteins after noise exposure likely contributes to the prevalence of survival cellular pathways and thus to the resistance to NIHL that is characteristic of the 129X1/SvJ mice. Keywords: effects of noise exposure in distinct inbred mice
2008-09-01 | GSE8342 | GEO
Project description:Mytilus edulis Vibrio bacterial challenge following noise exposure
| PRJEB91723 | ENA
Project description:Mytilus edulis Vibrio bacterial challenge following noise exposure
| PRJEB91724 | ENA
Project description:Lateral olivocochlear neurons modulate cochlear responses to noise exposure
| PRJNA1153007 | ENA
Project description:The study comprises of 24 subjects that have been exposed to low (H) and high dose (O) ambient traffic pollution. Each subject has been exposed to 2 different exposure site. Blood samples were taken at both sites of which circulating miRNAs in plasma have been prepared
2018-02-06 | GSE106221 | GEO
Project description:Six month-old wild type and Igf1 heterozygous mice were exposed to a violet swept sine noise (frequency range 2–20 kHz) at 110 dB SPL for 30 minutes. Cochlear samples were taken at 2 and 24 hours post-noise exposure to study the evolution of the expression of inflammation genes by using PCR arrays and RT-qPCR. Six month-old wild type and Igf1 heterozygous mice not exposed to noise were used as control.
2017-11-09 | GSE106667 | GEO