DNA microarray expression analysis of mice spleen following cadmium exposure
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PROVIDER: PRJNA529388 | ENA |
REPOSITORIES: ENA
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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
Project description:Few works have addressed the effects provoked by the exposure to cadmium containing nanoparticles (NPs) on adult zebrafish (Danio rerio). We studied the effects of CdS NPs (5 nm) or ionic cadmium (10 µg Cd/L) after 3 and 21 d of exposure and at 6 months post-exposure (mpe). Acute toxicity was recorded after exposure to both forms of cadmium. Significant cadmium accumulation was measured in the whole fish after both treatments and autometallography showed a higher accumulation of metal in the intestine than that in the liver. Histopathological alterations, such as inflammation in gills and vacuolization in the liver, were detected after the exposure to both cadmium forms and, in a lower extent, at 6 mpe. X-ray analysis proved the presence of CdS NPs in these organs. The hepatic transcriptome analysis revealed that gene ontology terms such as “immune response” or “actin binding” were over-represented after 21 d of exposure to ionic cadmium respect to CdS NPs treatment. Exposure to CdS NPs caused a significant effect on pathways involved in the immune response and oxidative stress, while the exposure to ionic cadmium affected significantly pathways involved in DNA damage and repair and in the energetic metabolism. Oxidative damage to liver proteins was detected after the exposure to ionic cadmium, while a stronger destabilization of the hepatocyte lysosomal membrane was recorded under exposure to CdS NPs. In summary, although ionic cadmium provoked stronger effects than CdS NPs, both cadmium forms exerted an array of lethal and sublethal effects to zebrafish.
2019-05-31 | GSE89756 | GEO
Project description:Obesity is considered as a major public health concern with strong economic and social burdens. Exposure to pollutants such as heavy metals can contribute to the development of obesity and its associated metabolic disorders, including type 2 diabetes and cardiovascular diseases. Adipose tissue is an endocrine and paracrine organ that plays a key role in the development of these diseases and is one of the main target of heavy metal accumulation. In this study, we determined by inductively coupled plasma mass spectrometry cadmium concentrations in human subcutaneous and visceral adipose tissues, ranging between 2.5 nM and 2.5 µM. We found a positive correlation between cadmium levels and age, sex and smoking status and a negative correlation between cadmium and body mass index. Based on cadmium adipose tissue concentrations found in humans, we investigated the effects of cadmium exposure, at concentrations between 1 nM and 10 µM, on adipose-derived human mesenchymal stem cells differentiated into mature adipocytes in vitro. Transcriptomic analysis highlighted that such exposure altered the expression of genes involved in trace element homeostasis and heavy metal detoxification, such as Solute Carrier Family transporters and metallothioneins. This effect correlated with zinc level alteration in cells and cellular media. Interestingly, dysregulation of zinc homeostasis and transporters has been particularly associated with the development of obesity and type 2 diabetes. Moreover, we found that cadmium exposure induces the pro-inflammatory state of the adipocytes by enhancing the expression of genes such as IL-6, IL-1B and CCL2, cytokines also induced in obesity. Finally, cadmium modulates various adipocyte functions such as the insulin response signaling pathway and lipid homeostasis. Collectively, our data identified some of the cellular mechanisms by which cadmium alters adipocyte functions, thus highlighting new facets of its potential contribution to the progression of metabolic disorders.
2023-06-29 | MTBLS4128 | MetaboLights
Project description:Cadmium is a metalloestrogen known to activate the estrogen receptor and promote breast cancer cell growth. Previous studies have implicated cadmium in the development of more malignant tumors; however the molecular mechanisms behind this cadmium-induced malignancy remain elusive. Using clonal cell lines derived by exposing breast cancer cells to cadmium for over 6 month (MCF7-Cd4, -Cd6, -Cd7, -Cd8 and -Cd12), this study aims to identify gene expression signatures associated with chronic cadmium exposure. Our results demonstrate that prolonged exposure does not merely result in the deregulation of genes but actually leads to a distinctive expression profile. The genes deregulated in cadmium-exposed cells are involved in multiple biological processes (i.e cell growth, apoptosis, etc.) and molecular functions (i.e. cadmium/metal ion binding, transcription factor activity, etc). Hierarchical clustering demonstrates that the five clonal cadmium cell lines share a common gene expression signature of breast cancer associated genes, clearly differentiating control from cadmium exposed cells. The results presented in this study offer insights into the cellular and molecular impacts of cadmium on breast cancer carcinogenesis and emphasize the importance of studying chronic cadmium exposure as one possible mechanism of promoting breast cancer progression. To understand the effects of chronic cadmium exposure on gene expression in breast cancer, two control MCF7 parental cell lines and five different clonal cadmium-adapted cell lines (MCF7-Cd4, -Cd6, -Cd7, -Cd8, and -Cd12) - previously derived from cells chronically exposed to cadmium - were used for microarray analysis.
2013-11-16 | E-GEOD-52404 | biostudies-arrayexpress
Project description:Cadmium is a metalloestrogen known to activate the estrogen receptor and promote breast cancer cell growth. Previous studies have implicated cadmium in the development of more malignant tumors; however the molecular mechanisms behind this cadmium-induced malignancy remain elusive. Using clonal cell lines derived by exposing breast cancer cells to cadmium for over 6 month (MCF7-Cd4, -Cd6, -Cd7, -Cd8 and -Cd12), this study aims to identify gene expression signatures associated with chronic cadmium exposure. Our results demonstrate that prolonged exposure does not merely result in the deregulation of genes but actually leads to a distinctive expression profile. The genes deregulated in cadmium-exposed cells are involved in multiple biological processes (i.e cell growth, apoptosis, etc.) and molecular functions (i.e. cadmium/metal ion binding, transcription factor activity, etc). Hierarchical clustering demonstrates that the five clonal cadmium cell lines share a common gene expression signature of breast cancer associated genes, clearly differentiating control from cadmium exposed cells. The results presented in this study offer insights into the cellular and molecular impacts of cadmium on breast cancer carcinogenesis and emphasize the importance of studying chronic cadmium exposure as one possible mechanism of promoting breast cancer progression.
2013-11-16 | GSE52404 | GEO
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
Project description:To understand how chronic cadmium exposure alters the dependency of ERα in terms of gene expression, we transiently silenced ERα using ICI, an antiestrogen that promotes the degradation of ERα. MCF7 and cadmium-adapted cells (Cd7 and Cd12) were treated with ICI to mediate the degradation of ERα, and a nonbiased global gene expression analysis was conducted using RNA-seq. MCF7 shared 67.3% and 59.5% of the DE genes with Cd7 and Cd12 cells, respectively, suggesting that ERα continues to play an important role in regulating the expression of genes following chronic cadmium exposure. 138 ERE genes (76.7%) were shared by all three cell lines, in that expression changed in the same direction (either up- or downregulated). For the estrogen-responsive genes, 428 (53.6%) of the 799 genes were altered in the same direction in all three cell lines. These findings show that while a majority of ERE genes responded in the same manner to loss of ERα, more variability existed within the estrogen-responsive genes. Collectively, these results indicate that while chronic cadmium exposure leads to genome-wide transcriptional changes, ERα remains important for regulating the expression of genes and maintaining the malignant phenotypes associated with breast cancer progression.
2019-08-21 | GSE134127 | GEO
Project description:Cadmium accumulation in kidney results in an irreversible chronic toxicity, but the underlying mechanisms are not clear. Transcriptomics assay may provide insight for the involved complex molecular networks. We used Affymetrix RTA arrays to detail the global gene expression profile of kidney tissues of SD rats with chronic exposure to Cadmium, and identified distinct classes of cadmium exposure related mRNA and pathways.
2022-12-31 | GSE109849 | GEO
Project description:BACKGROUND: Cadmium (Cd) is implicated in prostate carcinogenesis but its oncogenic action remains unclear. OBJECTIVES: This study aims to decipher changes in cell growth and the transcriptome in an immortalized human normal prostate epithelial cell line (NPrEC) following exposure to low-dose Cd. METHODS: Synchronized NPrEC cells were exposed to different doses of Cd and assayed for cell viability and cell-cycle progression. Temporal changes in transcriptome were investigated by global profiling. Ingenuity Pathways Analyses were used to develop propositions about functional connections among differentially expressed genes. A neutralizing antibody was used to negate the effect of Cd-induced upregulation of TNF in NPrEC. RESULTS: Exposure of NPrEC to 2.5 microM of Cd enhanced cell viability and accelerated cell-cycle progression. Global expression profiling identified 48 genes that exhibited â?¥1.5-fold changes in expression after 4, 8, 16 and 32 hr of Cd treatment. Pathway analyses inferred a functional connection among 35 of these genes in one major network with TNF as the most prominent node. Fourteen out of the 35 genes in the network are related to TNF with 11 exhibited an average of â?¥2-fold changes in gene expression. Real-time RT-PCR confirmed the upregulation of 7 of the 11 genes (ADAM8, EDN1, IL8, IL24, IL13RA2, COX2/PTGS2 and SERPINB2) and uncovered a 28-fold transient increase in TNF expression in Cd-treated NPrEC. A TNF-neutralizing antibody effectively blocked Cd-induced elevations in the expression of these genes. CONCLUSIONS: Non-cytotoxic, low-dose Cd has growth-promoting effects on NPrEC and induces transient overexpression of TNF, leading to upregulation of genes with oncogenic and immunomodulation functions. Experiment Overall Design: A total of 19 samples were analyzed, each experimental condition having two biological replicates, except Cadmium 4hr which has only 1 sample. Cadmium-treated and control samples were taken at 0, 4, 8, 16, and 32 hours.
2008-04-06 | E-GEOD-9951 | biostudies-arrayexpress
Project description:Cadmium is a natural element that can accumulate to toxic levels in the environment leading to detrimental effects in animals and humans including kidney, liver and lung injuries. Using a transcriptomics approach, genes and cellular pathways affected by a low dose of cadmium were investigated. Adult largemouth bass were intraperitoneally injected with 20 µg/kg of cadmium chloride and microarray analyses were conducted in the liver and testis 48 hours after injection. Transcriptomics profiles identified in response to cadmium treatment were tissue-specific with the most differential expression changes found in the liver tissues, which also contained much higher levels of cadmium than the testes. Acute exposure to a low dose of cadmium induced oxidative stress response and oxidative damage pathways in the liver. The mRNA levels of antioxidants such as catalase increased and numerous transcripts related to DNA damage and DNA repair were significantly altered. Hepatic mRNA levels of metallothionein, a proposed marker of cadmium exposure, showed a small insignificant increase after 48 hours exposure. Carbohydrate metabolic pathways were also disrupted in cadmium-exposed fish with hepatic transcripts such as UDP-glucose pyrophosphorylase 2 and sorbitol dehydrogenase highly induced. Both tissues exhibited a disruption of steroid signalling pathways. In the testis, estrogen receptor beta and transcripts linked to cholesterol metabolism were suppressed. On the contrary, genes involved in cholesterol metabolism were highly increased in the liver including genes encoding for the rate limiting steroidogenic acute regulatory protein and the catalytic enzyme 7-dehydrocholesterol reductase. Integration of the transcriptomics data using functional enrichment analyses revealed a number of enriched gene networks associated with previously reported adverse outcomes of cadmium exposure such as liver toxicity and impaired reproduction.
2014-04-02 | GSE53047 | GEO