Prenatal cadmium exposure alters proliferation in mouse CD4+ T cells via LncRNA Snhg7
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ABSTRACT:
PROVIDER: PRJNA733679 | ENA |
REPOSITORIES: ENA
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Project description:Prenatal cadmium (Cd) exposure leads to immunotoxic phenotypes in the offspring. Long non-coding RNAs (lncRNAs) are integral to T cell regulation. Here, we identified genes and pathways altered in CD4+ T cell by prenatal Cd exposure. We investigated the role of long non-coding RNA small nucleolar RNA hostgene 7 (lncSnhg7) in T cell proliferation: LncSnhg7 expression increases in CD4+ T cells following stimulation with anti-CD3/CD28 beads. LngSnhg7 and a downstream protein, GALNT7, are upregulated in T cells from offspring exposed to Cd during gestation. Overexpression of miR-34a, a regulator of lnhcSnhg7 and GALNT7, suppresses GALNT7 protein levels in primary T cells, but not in a mouse T lymphocyte cell line. The T cells isolated from Cd-exposed offspring exhibit increased proliferation after activation in vitro, but Treg suppression and CD4+ T cell apoptosis are not affected by prenatal Cd exposure. In conclusion, prenatal Cd exposure alters the expression of lncRNAs during T cell activation. The induction of lncSnhg7 is enhanced in splenic T cells from Cd offspring resulting in the upregulation of GALNT7 protein and increased proliferation following activation. miR-34a overexpression decreased GALNT7 expression suggesting that the lncSnhg7/miR-34a/GALNT7 is an important pathway in primary CD4+ T cells. These data highlight the need to understand the consequences of environmental exposures on lncRNA functions in non-cancerous cells.
2021-12-23 | GSE175796 | GEO
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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
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Project description:In our lab, Cadmium treatment of human fibroid cells induced a cancer phenotype and altered glycogen metabolism. In this study we treated fibroid cells with cadmium continuously for 2 or 6 months. Cancer progression and pathway gene expression were investigated using NanoString Technologies.
2021-10-29 | GSE178789 | GEO
Project description:In our lab, Cadmium treatment of human fibroid cells induced a cancer phenotype and altered glycogen metabolism. In this study we treated fibroid cells with cadmium continuously for 2 or 6 months. Cancer progression and pathway gene expression were investigated using NanoString Technologies.
2021-10-29 | GSE178786 | GEO
Project description:Cadmium is a heavy metal pollutant and environmental endocrine disruptor. Studies have shown that cadmium exposure, whether it occurs in adulthood, in puberty or during the period from weaning to sexual maturity, can produce notable toxic effects on ovarian cells, especially ovarian granulosa cells. However, the effects of prenatal cadmium exposure on the morphology, function and its epigenetic mechanism of ovarian granulosa cells in offspring during adulthood have not been reported.In this study,the promoter methylation was assessed using MeDIP-Chip and Several methods were used to analyze the scanned genes, including the Gene Ontology Consortium tools, hierarchical clustering and KEGG pathway analysis.The results indicated that multiple signaling pathways, including apoptosis and hormone synthesis related pathways were affected,besides, some genes DNA methylation status of apoptosis and hormone synthesis pathways were changed.In summary, our results provide a scientific basis for subsequent analyses of cadmium-induced ovarian granulosa cell damage and its epigenetic mechanism.
2022-02-01 | GSE127254 | 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: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:We investigated the hormetic effects of prenatal hyperbaric normoxia exposure on Drosophila healthspan related to molecular defense mechanisms. HN exposure had no disruptive effect on developmental rate or adult body weight. However, lifespan was clearly enhanced, as was resistance to oxidative and heat stress. In addition, levels of reactive oxygen species were significantly decreased and motor performance was increased. Furthermore, to determine the hormetic mechanism underlying these phenotypic and molecular changes, we performed a genome-wide profiling in HN-exposed and control flies. Genes encoding chitin metabolism were highly up-regulated in both sex, which could possibly serve to scavenge free radicals. These results identify prenatal HN exposure as a potential hormetic factor that may improve longevity and healthspan by enhancing defense mechanisms in Drosophila.
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