Chronic cadmium exposure induces differential methylation in mice spermatozoa
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA665258 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We used Reduced Representation Bisulfite Sequencing (RRBS) to comprehensively investigate the impact of chronic, low-dose Cd exposure on mice spermatozoa DNA methylation. Adult male C57BL/J6 mice were provided water with or without cadmium chloride. We purified genomic DNA from sperm samples collected after nine weeks of treatment. We found 1,788 differentially methylated sites present at regulatory regions in sperm of mice exposed to chronic, low-dose of Cd compared to vehicle (control) mice. Our results present a comprehensive analysis of the sperm methylome in response to chronic Cd exposure
2021-01-25 | GSE158455 | GEO
Project description: Not available
| S-EPMC8041459 | biostudies-literature
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 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: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: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:Systemic hormonal modulation induces sperm nucleosomal imbalance in rat spermatozoa
| PRJNA431405 | ENA
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
Project description: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.
2022-03-06 | GSE189530 | GEO