Differential Expression Profiles and Potential Intergenerational Functions of tRNA-Derived Small RNAs in Mice After Cadmium Exposure
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA786488 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17139513.fastq.gz | Fastqsanger.gz | |||
| SRR17139514.fastq.gz | Fastqsanger.gz | |||
| SRR17139515.fastq.gz | Fastqsanger.gz | |||
| SRR17139516.fastq.gz | Fastqsanger.gz | |||
| SRR17139517.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Cadmium (Cd) is a toxic heavy metal and ubiquitous environmental endocrine disruptor. Previous studies on Cd-induced damage to male fertility mainly focus on the structure and function of testis, and semen quality. Nevertheless, to date, no studies have investigated the effects of Cd exposure on sperm epigenetic inheritance and intergenerational inheritance. In our study, we systematically revealed the changes in sperm tRNA-derived small RNAs (tsRNA) profiles and found that 14 tsRNAs (9 up-regulated and 5 down-regulated) were significantly altered after Cd exposure. Bioinformatics of tsRNA-mRNA-pathway interactions revealed that the altered biological functions mainly were related to ion transmembrane transport, lipid metabolism and cell membrane system. In addition, we focused on two stages of early embryo development and selected two organs to study the impact of these changes on cell membrane system, especially mitochondrion and lysosome, two typical membrane-enclosed organelles. Surprisingly, we found that the content of mitochondrion was significantly decreased in 2-cell stage, whereas remarkably increased in the morula stage. The contents of mitochondrion and lysosome were significantly increased in the testes of 6-days offspring and livers of adult offspring, whereas remarkably decreased in the testes of adult offspring. This provides a possible basis to further explore the effects of paternal Cd exposure on offspring health.
2021-12-15 | GSE190236 | GEO
Project description:Cadmium (Cd) is a toxic heavy metal and ubiquitous environmental endocrine disruptor. Previous studies on Cd-induced damage to male fertility mainly focus on the structure and function of testis, including cytoskeleton, blood-testis barrier, and steroidogenesis. Nevertheless, to date, no studies have investigated the effects of Cd exposure on sperm epigenetic inheritance and intergenerational inheritance. In our study, we systematically revealed the changes in sperm tRNA-derived small RNAs (tsRNA) profiles and found that 14 tsRNAs (9 up-regulated and 5 down-regulated) were significantly altered after Cd exposure. Bioinformatics of tsRNA-mRNA-pathway interactions revealed that the altered biological functions mainly were related to ion transmembrane transport, lipid metabolism and cell membrane system. In addition, we focused on two stages of early embryo development and selected two organs to study the impact of these changes on cell membrane system, especially mitochondrion and lysosome, two typical membrane-enclosed organelles. Surprisingly, we found that the content of mitochondrion was significantly decreased in 2-cell stage, whereas remarkably increased in the morula stage. The contents of mitochondrion and lysosome were increased in the testes of 6-day-old offspring and livers of adult offspring, whereas remarkably decreased in the testes of adult offspring. This provides a possible basis to further explore the effects of paternal Cd exposure on offspring health.
| S-EPMC8762212 | 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.
2013-11-16 | GSE52404 | 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. 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:These data demonstrate that parental exposure to bacterial infection and osmotic stress intergenerational changes in offspring gene expression in C. elegans, C. kamaaina, C. briggsae and C. tropicalis. Many of these intergenerational changes in gene expression are observed in multiple species and this data identified >250 genes that exhibit intergenerational changes in expression in all species tested.
2021-05-07 | GSE173987 | 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:tRNA-derived fragments (tRFs) have served as new class of non-coding RNA and played important role in regulating cellular RNA processing and protein translation, which was also proved have function on the intergenerational effects of paternal disease. However, there was no study reported the influence of tRFs on myocardial hypertrophy. In the current study, we explore the hypothesis that tRFs in response to myocardial hypertrophy and contribute to intergenerational inheritance.We used isoproterenol induced myocardial hypertrophy rat model. Small RNA (< 40 nt) tanscriptome sequencing was used to select differential expressed tRFs. We over-expressed the highest foldchange tRFs on H9c2 cell to check its function in enlarging cardiocytes surface area. We also compared the tRFs expression pattern in F0 sperm and F1 offspring heart between myocardial hypertrophy (Hyp) and control group (Con), as well as evaluated the phynotype of myocardial hypertrophy in F1 offspring. ISO successfully induced a typical cardiac hypertrophy model in our study. Small RNA-seq revealed tRFs were extremely enriched (84%) in Hyp heart. Overexpression tRFs1 and tRFs2 would both enlarge the surface area of cardiac cell and increase hypertrophic markers (ANF, BNP, and β-MHC) expression. tRFs1, tRFs2, tRFs3 and tRFs4 were also significantly high expressed in Hyp F0 sperm and in Hyp F1 offspring heart, but no function of tRFs7, tRFs9 and tRFs10. Compared to Con F1 offspring, Hyp F1 offspring had high expression levels of β-MHC and ANP genes, and increased fibrosis levles and apoptotic cell in heart.We demonstrate that tRFs are involved in regulating the response of myocardial hypertrophy, it might serve as novel epigenetic factor and contribute to intergenerational inheritance of cardiac hypertrophy.
2017-11-04 | GSE106511 | GEO
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:Intergenerational genomic DNA methylation patterns in mouse hybrid strains Reduced representation bisulfite sequencing from mouse liver, using MspI restriction enzyme, and selecting ~100-300bp size fraction.
2013-12-30 | E-GEOD-53714 | biostudies-arrayexpress