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Deep learning approach identified a gene signature predictive of the severity of renal damage caused by chronic cadmium accumulation

ABSTRACT: Repetitive CdCl2 exposure resulted in cadmium accumulation and remarkable renal injuries in the animals. In the present study, we established an animal model to mimic chronic cadmium exposure-induced renal injury and performed whole transcriptome profiling studies. RNA-Seq data analysis showed that cadmium treatment induced dramatic gene expression changes in kidneys in a dose-dependent manner and higher severity of injury in ob/ob mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE189530 | GEO | 2022/03/06

REPOSITORIES: GEO

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METTL3-mediated m6A mRNA modification was involved in cadmium-induced liver disease

Project description:Cadmium is an environmental pollutant that has extensive deleterious effects. However, the mechanisms underlying the hepatotoxicity induced by long-term exposure to cadmium remained undefined. In the present study, we explored the role of m6A methylation in the development of cadmium-induced liver disease. We showed a dynamic change of RNA methylation in liver tissue from mice administrated with cadmium chloride (CdCl2) for 3, 6 and 9 months, respectively. Particularly, the METTL3 expression was declined in a time-dependent manner, associated with the degree of liver injury, indicating the involvement of METTL3 in hepatotoxicity induced by CdCl2. Moreover, we established a mouse model with liver-specific over-expression of Mettl3 and administrated these mice with CdCl2 for 6 months. Notably, METTL3 highly expressed in hepatocytes attenuated CdCl2-induced steatosis and liver fibrosis in mice. In vitro assay also showed METTL3 overexpression ameliorated the CdCl2-induced cytotoxicity and activation of primary hepatic stellate cells. Furthermore, transcriptome analysis identified 268 differentially expressed genes both in mice liver tissue treated with CdCl2 for 3 months and 9 months. Among them, 115 genes were predicted to be regulated by METTL3 determined by m6A2Target database. Further analysis revealed the perturbation of metabolic pathway, glycerophospholipid metabolism, ErbB signaling pathway, Hippo signaling pathway, and choline metabolism in cancer, and circadian rhythm, led to hepatotoxicity induced by CdCl2. Collectively, our findings reveal new insight into the crucial role of epigenetic modifications in hepatic diseases caused by long-term exposure to cadmium.

2023-06-30 | GSE230188 | GEO

DNA microarray expression analysis of mice spleen following cadmium exposure

Project description:This study use DNA microarray to examine gene expression in the spleen of mice exposed to cadmium. Mice were exposed via a single subcutaneous injection CdCl2, with spleen harvested at 24h after exposure for microarray analysis. This work provides insight into the mechanistic pathways involved in acute cadmium intoxication, providing a theoretical basis for identifying candidate biomarkers.

2019-03-28 | GSE128931 | GEO

cadmium-mirna-cadmium stress on suspension cells.

Project description:rs06-03_cd-mirna - cadmium-mirna - trancriptional and post-transcriptional response to cadmium. - After 5 days of grown in a fresh medium (5% PCV at day0), CdCl2 was added to tested cells (Cad) to a final concentration of 200uM. Nothing was added to control cells (Tem). After 12 and 24 hours of growth +/- cadmium, cells were harvested and frozen in liquid nitrogen.

2012-03-25 | GSE36627 | GEO

cadmium-mirna-cadmium stress on suspension cells.

2012-03-25 | E-GEOD-36627 | biostudies-arrayexpress

Cadmium chloride-induced gene expression changes in D. melanogaster

Project description:Heavy metals and organic compounds, such as pesticides and plasticizers, exert toxicity through their ability to perturb molecular mechanisms. We investigated the ability of 18 compounds to modify the epigenetic state of the white locus in a Drosophila model of position-effect variegation (PEV). Our data indicate that cadmium chloride (CdCl2) is a potent enhancers of variegation. We demonstrate that genes differentially expressed upon CdCl2 exposure are enriched for genes that have heterochromatic states associated with them.

2019-08-01 | GSE118536 | GEO

Transcriptome Analysis of North Atlantic Right Whale Kidney Fibroblast Cell line exposed to cadmium

Project description:An 8X15k oligonucleotide microarray was developed consisting of 2334 E. glacialis probes and 2166 Tursiops truncatus probes and used to measure the transcriptome level effects of right whale kidney fibroblast cells exposed to cadmium. Cells were exposed to three concentrations of cadmium chloride (CdCl2) for three exposure times. Cells exposed to 10-6M CdCl2 for 4 hours and 24 hours showed upregulated genes involved in protection from metal toxicity, oxidative stress, protein renaturation, apoptosis inhibition, and several regulators of cellular processes. Downregulated genes represented a suite of functions including cell proliferation, transcription regulation, actin polymerization, and stress fiber synthesis. The collection of differentially expressed genes in this study support proposed mechanisms of cadmium-induced apoptosis such as mitochondrial membrane potential collapse, reactive oxygen species (ROS) influx, and cell cycle arrest. The results confirm the right whale microarray as a reproducible tool in measuring differentiated gene expression and should be a valuable asset for transcriptome analysis of other baleen whales and potential health assessment protocols.

2009-08-03 | GSE17457 | GEO

Impaired PPARɣ activation by cadmium exacerbates infection-induced lung injury

Project description:Emerging data indicates an association between environmental heavy metal exposure and lung disease, including lower respiratory tract infections (LRTIs). Here, we show by single cell RNA-sequencing an increase in Pparg gene expression in lung macrophages from mice exposed to cadmium and/or infected with S. pneumoniae. However, the heavy metal cadmium or infection mediated an inhibitory post-translational modification of peroxisome proliferator-activated receptor ɣ (PPARɣ) to exacerbate LRTIs. Cadmium and infection increased ERK activation to regulate PPARɣ degradation in monocyte-derived macrophages. Mice harboring a conditional deletion of Pparg in monocyte-derived macrophages had more severe S. pneumoniae infection after cadmium exposure, showed greater lung injury, and had increased mortality. Inhibition of ERK activation with BVD-523 protected mice from lung injury after cadmium exposure or infection. Moreover, subjects residing in areas of high air cadmium levels had increased cadmium concentration in their BAL fluid and showed PPARɣ inhibition that was mediated, at least in part, by ERK activation in isolated BAL cells. These observations suggest that impaired activation of PPARɣ in monocyte-derived macrophages exacerbates lung injury and the severity of LRTIs.

2023-09-07 | GSE225386 | GEO

Genome-Wide Transcriptional Responses of Nitrosomonas europaea to cadmium

Project description:Heavy metals have been postulated as significant nitrification inhibitor in wastewater treatment plant. The effect of heavy metals such as Cd2+, Cu2+ and Hg2+ to nitrifying bacterium, Nitrosomonas europaea, was studied in pseudo-steady state batch reactor. Under incubation of Nitrosomonas europaea with 1 ?M CdCl2 for 1 hour, transcripts for 66 of 2460 genes were found at high level, yet transcripts of 50 genes were found at low level. Mercury resistance genes (merACDPT) showed 277-fold up regulation. Keywords: cadmium, stress response, global transcription, mercury resistance genes, merA, The 1 uM CdCl2 caused more than 50 % inhibition in physiological response for 1 hour incubation. Transcriptional levels of the cells inhibited by cadmium were compared with the cells under control condition.

2010-05-25 | E-GEOD-9221 | biostudies-arrayexpress

Liver transcript expression patterns in the sparid striped seabream (Lithognathus mormyrus) upon exposure to cadmium

Project description:Changes in hepatic gene expression profiles upon exposures to cadmium applied by feeding or intra-peritoneal injections were identified in the striped sea bream (Lithognathus mormyrus) using cDNA microarray platform. Two groups of four fish were exposed to fed and injected CdCl2, respectively. Additional eight untreated fish were used as a reference group, pooled into 4 hepatic RNA preparations. The isolated hepatic mRNAs were hybridized, after conversion to labeled cDNAs, onto the microarray followed by slide scanning, imaging and analysis. Four parameters: M, meanA, P-value and B were calculated for each unique spot, for both cadmium-fed vs. reference fish (sample1) and cadmium-injected vs. reference fish (sample2). These parameters enable evaluation of hybridization intensity as well as statistical testing of differential expression. Keywords: Response to exposure to cadmium

2007-12-26 | GSE8005 | GEO

Cadmium exposure induces SNAIL1 expression via downregulation of miR-30e in human bronchial epithelial cells

Project description:Purpose: To understand the molecular mechanisms underlying Cd exposure-induced diseases. Methods: Immortalized human bronchial epithelial cells (BEAS-2B) were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Cellgro) supplemented with 1% Penicillin Streptomycin and 10% Fetal Bovine Serum (FBS, Atlanta Biologicals) at 37 degree C and 5 % CO2. For Cd exposure, 0, 2.5, 5 and 10 µM of CdCl2 was added to the media and the cells were cultured for 72h. Results: This study shows that cadmium exposure induces SNAIL1 expression via miR-30e downregulation and the cells undergo epithelial-mesenchymal transition.

2019-06-16 | GSE128263 | GEO

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