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Cadmium-mirna-cadmium stress on suspension cells.

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE36627 | GEO | 2012/03/25

SECONDARY ACCESSION(S): PRJNA156685

REPOSITORIES: GEO

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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. 4 dye-swap - treated vs untreated comparison

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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.

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