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Perturbation of epigenetic processes by doxorubicin in the mouse testes: microRNA analysis

ABSTRACT: microRNA profiling of mouse testis comparing treatment with doxorubicin to vehicle only control (published in Toxicology Research, DOI: 10.1039/C6TX00078A)

ORGANISM(S): Mus musculus

PROVIDER: GSE83661 | GEO | 2016/06/24

SECONDARY ACCESSION(S): PRJNA326666

REPOSITORIES: GEO

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Perturbation of epigenetic processes by doxorubicin in the mouse testes: mRNA analysis

Project description:mRNA profiling of mouse testis comparing treatment with doxorubicin to vehicle only control (published in Toxicology Research, DOI: 10.1039/C6TX00078A)

2016-08-04 | GSE85140 | GEO

Perturbation of epigenetic processes by doxorubicin in the mouse testes: microRNA analysis

Project description:microRNA profiling of mouse testis comparing treatment with doxorubicin to vehicle only control (published in Toxicology Research, DOI: 10.1039/C6TX00078A) Two-condition experiment, doxorubicin vs control at 3 time points (1wk, 4wk and 7 wk following treatment). Biological replicates: 12 control, 12 doxorubicin (implementing a dye swap design of n=6 forward and n=6 reverse). One replicate per dual colour array (total of 36 arrays).

2016-06-24 | E-GEOD-83661 | biostudies-arrayexpress

Perturbation of epigenetic processes by doxorubicin in the mouse testes: mRNA analysis

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Perturbation of epigenetic processes by doxorubicin in the mouse testis.

Project description:Epigenetic processes play a major role in normal mammalian development, particularly during gametogenesis and early embryogenesis. Thus, perturbation of epigenetic processes in the testis by xenobiotics could have a major impact on testicular function and fertility, and potentially affect the development and health of subsequent generations. There has been substantial research into the epigenetic toxicity of environmental exposures over the last decade. However, few studies have focussed on pharmaceutical drugs, which due to the nature of their use are typically found at much higher concentrations within exposed individuals than environmental chemicals. Here, we investigated genome-wide changes in testicular mRNA transcription, microRNA expression and DNA methylation to assess the contribution of epigenetic mechanisms to the testicular toxicity induced by doxorubicin (DOX) as a representative, widely used and well-characterised anti-cancer drug. We demonstrated that DOX is able to induce transcriptional, microRNA and DNA methylation changes, which perturb pathways involved in stress/cell death and survival and testicular function and lead to germ cell loss and reproductive organ damage. This identified potential novel mechanisms of DOX-induced testicular toxicity for further focussed investigations. Such work is required to fully assess the role of epigenetics in toxicity, determine whether single and/or multigenerational epigenetic toxicity is a real public health concern, and begin to develop and incorporate relevant epigenetic endpoints into regulatory toxicology.

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Effects on gene expression of doxorubicin in human stem cells-derived cardiomyocytes

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Project description:To compare expression profiles in the cardiomyocytes with wild type top2b and those with top2b deletion after in vivo treatment of mice with doxorubicin or drug vehicle Doxorubicin is widely used in modern cancer treatments, despite the advent of targeted therapy. However, a dose-dependent cardiotoxicity often limits its clinical use. The prevailing theory hypothesizes that doxorubicin-induced cardiotoxicity is the result of reactive oxygen species (ROS) generation due to redox-cycling of doxorubicin. Here we showed that cardiomyocyte-specific deletion of Topoisomerase II beta (Top2b) markedly reduced DNA double-strand breaks, apoptosis, and functional damages in doxorubicin-treated hearts. To investigate transcriptomic changes after doxorubicin treatment in wild type mouse and mouse with cardiac specific deletion of Top2b, we examined the expression profiles in 4 groups of mice (3/group), ie. wildtype mice with or without doxorubicin treatment and mice with Top2b deletion in the cardiomyocytes with or without doxorubicin treatment. Mice were treated with doxorubicin (25mg/kg, i.p.) or PBS (drug vehicle) for 16 hr or 72 hr. The heart was removed and cardiomyocytes were isolated by using a Langendorff apparatus. After purification, total RNA was extracted from the cardiomyocytes, purified, and used for gene expression analysis. Compared with that in control cardiomyocytes or cardiomyocytes with Top2b deletion, doxorubicin caused a significant expression change in the genome of cardiomyocytes from the wildtype mice. Among the changes, multiple genes encoding mitochondrial structural protein and components of the respiratory chain complexes were down-regulated 72 hr after treatment while multiple genes in the p53 pathway were up-regulated 16 hr after treatment in the wildtype cardiomyocytes.

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