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Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

ABSTRACT: Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

PROVIDER: PRJNA1005939 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25655338_1.fastq.gz	Fastqsanger.gz
	SRR25655338_2.fastq.gz	Fastqsanger.gz
	SRR25655339_1.fastq.gz	Fastqsanger.gz
	SRR25655339_2.fastq.gz	Fastqsanger.gz
	SRR25655340_1.fastq.gz	Fastqsanger.gz

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Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

Project description:Wild-type (WT) and Otub1-heterozygously knock-out mice were applied in the study. Doxorubicin (DOX)-induced subacute cardiotoxicity mouse model was established by 6 intraperitoneal injections during a 2-week period. The differentially expressed genes were analyzed by RNA-sequencing and clustering analyses.

2024-08-16 | GSE240959 | GEO

Targets of miR-212/132 in doxorubicin-induced cardiotoxicity

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CRISPRi/a screen of doxorubicin induced cardiotoxicity

Project description:CRISPRi/a screen of doxorubicin induced cardiotoxicity

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Transcriptional analysis of doxorubicin-induced cardiotoxicity

Project description:Doxorubicin (Dox) is an effective chemotherapeutic agent against a broad range of tumors. However, a threshold dose of doxorubicin causes an unacceptably high incidence of heart failure and limits its clinical utility. We have established two models of doxorubicin cardiotoxicity in mice: 1) in an acute model, mice are treated with 15mg/kg of doxorubicin once; 2) in a chronic model, they receive 3mg/kg weekly for the first 12 of a total of 18 weeks. Using echocardiography, we have monitored left ventricular function of the mouse hearts during treatment in chronic model and seen the expected development of dilated cardiomyopathy (DCM). Treated mice showed histological abnormalities similar to those seen in patients with doxorubicin cardiomyopathy. To investigate transcriptional regulation in these models, we used a microarray we generated with over 5000 independent cDNA clones from murine heart and skeletal muscle. We have identified genes that respond to doxorubicin exposure in both model systems, and confirmed these results using real-time PCR. In the acute model, a set of genes is regulated early and rapidly returns to baseline levels, consistent with the half-life of doxorubicin. In the chronic model, which mimics the clinical situation much more closely, we identified dysregulated genes that implicate specific mechanisms of cardiac toxicity and may serve as biomarkers of doxorubicin induced dilated cardiomyopathy. Keywords: time course

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Transcriptomic analysis of folic acid effects in doxorubicin-induced cardiotoxicity

Project description:Doxorubicin (DOXO), a chemotherapeutic drug, is cardiotoxic. We hypothesized that folic acid is an effective therapeutic agent in a mouse model of DOXO-induced cardiotoxicity. We performed genome-wide expression profiling to identify the underlying mechanisms. Male C57Bl6 2-mo old mice received DOXO (1x20 mg/kg, ip) or saline (sham). FA (10 mg/d) or placebo (plac) was administered 7d before DOXO administration until the end of the experiment (10d).

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The Cardiac Endothelial Cell cGAS-STING Pathway Promotes Doxorubicin-Induced Cardiotoxicity via CD38-Mediated NAD Decline and Mitochondrial Dysfunction [human]

Project description:Doxorubicin is an effective chemotherapy drug for treating various types of cancer. However, lethal cardiotoxicity severely limits its clinical use. Recent evidence has indicated that aberrant activation of the cytosolic DNA-sensing cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a critical role in cardiovascular destruction. Here, we investigate the involvement of this mechanism in doxorubicin-induced cardiotoxicity (DIC).

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The Cardiac Endothelial Cell cGAS-STING Pathway Promotes Doxorubicin-Induced Cardiotoxicity via CD38-Mediated NAD Decline and Mitochondrial Dysfunction [mouse]

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Phosphodiesterase 10A inactivation protects against doxorubicin-induced cardiotoxicity and concomitantly inhibits tumor growth

Project description:Phosphodiesterase 10A (PDE10A), by degrading cAMP/cGMP, play critical roles in cardiovascular biology/disease. Cardiotoxicity is a clinical complication of chemotherapy. We aim to determine the role of PDE10A in cancer growth and cardiotoxicity induced by doxorubicin (DOX), a chemotherapy drug. We found that PDE10A deficiency/inhibition alleviated DOX-induced cardiotoxicity in C57Bl/6J mice, including myocardial atrophy, apoptosis, and dysfunction. RNAseq study revealed several PDE10A-regulated signaling associated with DOX-induced cardiotoxicity. In cancer cells, PDE10A inhibition increased the death, decreased the proliferation, and potentiated the effect of DOX in various cancer-cell lines. Importantly, in nude mice with implanted ovarian cancer xenografts, PDE10A inhibition attenuated tumor growth while protected against DOX-induced cardiotoxicity. In isolated cardiomyocytes (CMs), PDE10A contributed to DOX-induced CM death via promoting mitochondrial dysfunction, and to CM atrophy via potentiating foxo3 signaling. Collectively, our study elucidates a novel role for PDE10A in cardiotoxicity and cancer growth in vitro and in vivo, and suggest that PDE10A inhibition may represent a novel strategy in cancer therapy.

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Project description:Targets of miR-212/132 in doxorubicin-induced cardiotoxicity

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