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M6A Demethylase ALKBH5 attenuates doxorubicin-induced cardiotoxicity via posttranscriptional stabilization of Rasal3

ABSTRACT: m6A Demethylase ALKBH5 attenuates doxorubicin-induced cardiotoxicity via posttranscriptional stabilization of Rasal3

PROVIDER: PRJNA930335 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23300935_1.fastq.gz	Fastqsanger.gz
	SRR23300935_2.fastq.gz	Fastqsanger.gz
	SRR23300936_1.fastq.gz	Fastqsanger.gz
	SRR23300936_2.fastq.gz	Fastqsanger.gz
	SRR23300937_1.fastq.gz	Fastqsanger.gz

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m6A Demethylase ALKBH5 attenuates doxorubicin-induced cardiotoxicity via posttranscriptional stabilization of Rasal3

Project description:The clinical application of anthracyclines such as doxorubicin (DOX) is limited due to their cardiotoxicity. N6-methyladenosine (m6A) plays an essential role in numerous biological processes. However, the roles of m6A and m6A demethylase ALKBH5 in DOX-induced cardiotoxicity (DIC) remain unclear. In this research, DIC models were constructed using Alkbh5-knockout (KO), Alkbh5-knockin (KI), and Alkbh5-myocardial-specific knockout (ALKBH5flox/flox, αMyHC-Cre) mice. Cardiac function and DOX-mediated signal transduction were investigated. As a result, both Alkbh5 whole-body KO and myocardial-specific KO mice had increased mortality, decreased cardiac function, and aggravated DIC injury with severe myocardial mitochondrial damage. Conversely, ALKBH5 overexpression alleviated DOX-mediated mitochondrial injury, increased survival, and improved myocardial function. Mechanistically, ALKBH5 regulated the expression of Rasal3 in an m6A-dependent manner through posttranscriptional mRNA regulation and reduced Rasal3 mRNA stability, thus activating RAS3, inhibiting apoptosis through the RAS/RAF/ERK signaling pathway, and alleviating DIC injury. These findings indicate the potential therapeutic effect of ALKBH5 on DIC.

2023-03-08 | GSE224215 | GEO

m<sup>6</sup>A demethylase ALKBH5 attenuates doxorubicin-induced cardiotoxicity via posttranscriptional stabilization of Rasal3.

| S-EPMC9982307 | biostudies-literature

Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

Project description:Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

| PRJNA1005939 | ENA

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

Project description:We overexpressed miR-212/132 by AAV9 in mouse model of doxorubicin-induced cardiotoxicity and wanted to identify myocardial targets of miR-212/132 in this model.

2018-12-29 | GSE121965 | GEO

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).

2015-11-12 | E-GEOD-64476 | biostudies-arrayexpress

CRISPRi/a screen of doxorubicin induced cardiotoxicity

Project description:CRISPRi/a screen of doxorubicin induced cardiotoxicity

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Transcriptomic analysis of folic acid effects in doxorubicin-induced cardiotoxicity

2015-11-12 | GSE64476 | GEO

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

2005-07-22 | GSE2965 | GEO

Analysis of potential transcriptomic biomarkers for doxorubicin cardiotoxicity in peripheral blood

Project description:The aim of this study is the characterize and compare heart and PBMC transcriptomes of rats treated with doxorubicin in order to isolate a list of similarly differentially regulated genes with an ultimate goal to indentify PBMC biomarkers for early prediction of doxirubicinduced cardiotoxicity Total RNA was isolated from PBMC and hearts of rats treated with doxirubicin or saline for 48 hrs and used for gene expression

2013-12-31 | E-GEOD-37260 | biostudies-arrayexpress

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