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Metabolic conditioning enhances human bmMSC cell therapy of doxorubicin-induced heart failure

ABSTRACT: Metabolic conditioning enhances human bmMSC cell therapy of doxorubicin-induced heart failure

PROVIDER: PRJNA1055094 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27308200_1.fastq.gz	Fastqsanger.gz
	SRR27308200_2.fastq.gz	Fastqsanger.gz
	SRR27308201_1.fastq.gz	Fastqsanger.gz
	SRR27308201_2.fastq.gz	Fastqsanger.gz
	SRR27308202_1.fastq.gz	Fastqsanger.gz

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Metabolic conditioning enhances human bmMSC cell therapy of doxorubicin-induced heart failure

Project description:The therapeutic potential of bone marrow mesenchymal stromal cells (bmMSCs) in addressing heart failure need improvement for a better engraftment and survival. This study explores the role of metabolic sorting for human bmMSC on coculture in vitro and on doxorubicin-induced heart failure mice models. Using functional, epigenetic and gene expression approaches on cells sorted on the mitochondrial membrane potential referring their metabolic status, we demonstrated that bmMSC selected for their glycolytic metabolism presented proliferative advantage and resistance to oxidative stress favoring cell engraftment. Therapeutic use of glycolytic bmMSC rescued left ventricular ejection fraction and decrease fibrosis in mice model of acute heart failure. Metabolic changes were also related to epigenetic histone modifications as lysine methylation. Targeting LSD1 (lysine-specific demethylase 1) as a conditioning agent for enhancing the metabolic profile of bmMSC, we decipher the interplay between glycolysis and cell functionality. Our study leads to elucidate novel strategies for optimizing bmMSC-based therapies in treating heart failure and highlight the metabolic properties of bmMSCs as a promising target for more effective cardiovascular regenerative therapies.

2024-07-31 | GSE251709 | GEO

Doxorubicin enhances nucleosome turnover around promoters

Project description:We use a metabolic labeling strategy for directly measuring nucleosome turnover to examine the effect of doxorubicin on chromatin dynamics in squamous cell carcinoma cell lines derived from genetically defined mice. We find that doxorubicin enhances nucleosome turnover around gene promoters, and turnover correlates with gene expression level. Keywords: Chromatin affinity-purification on microarray 26 CATCH-IT arrays and 8 expression arrays.

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AICAR-cardioprotection in doxorubicin-induced heart failure in rats

Project description:AICAR-cardioprotection in doxorubicin-induced heart failure in rats

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Doxorubicin enhances nucleosome turnover around promoters

2013-04-19 | GSE43753 | GEO

AICAR-cardioprotection in doxorubicin-induced heart failure in rats

Project description:Doxorubicin (DOX) is a widely used chemotherapeutic agent that can cause serious cardiotoxic side effects, leading to functional cardiac decline and ultimately, congestive heart failure (HF). Impaired mitochondrial function and energetics are thought to be key factors driving progression into HF. We have previously shown in a rat model of chronic intravenous DOX-administration that heart failure with reduced ejection fraction correlates with mitochondrial loss and dysfunction. Adenosine monophosphate-dependent kinase (AMPK) is a cellular energy sensor, regulating mitochondrial biogenesis and oxidative metabolism, including fatty acid oxidation. We hypothesized that AMPK activation could restore mitochondrial number and function and therefore be a novel cardioprotective strategy for the prevention of DOX-HF. Consequently, we set out to assess whether 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR), an activator of AMPK, could prevent cardiac functional decline in this clinically relevant rat model of DOX-HF. In line with our hypothesis, AICAR improved cardiac systolic function. This was associated with normalisation of substrate supply to the heart, as AICAR prevented DOX-induced dyslipidaemia. AICAR furthermore improved cardiac mitochondrial fatty acid oxidation, independent of mitochondrial number. In addition, we found that AICAR reduced the degree of myocardial atrophy, and RNAseq analysis showed that this was driven by normalisation of protein synthesis pathways, which are impaired in DOX-treated rat hearts. Taken together, these results show promise for the use of AICAR as a cardioprotective agent in DOX-HF to both preserve cardiac function and mass.

2024-11-01 | GSE218397 | GEO

Targeting mitochondrial metabolism for detection and treatment of doxorubicin-induced heart failure

Project description:Targeting mitochondrial metabolism for detection and treatment of doxorubicin-induced heart failure

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Targeting mitochondrial metabolism for detection and treatment of doxorubicin-induced heart failure

Project description:We conducted RNAseq using mRNA extracted from rat hearts to elucidate the effect of doxorubicin chemotherapy on the heart. Rats were 250g at the start of the treatment protocol. Tissues were collected post five weekly intravenous injections of either sterile saline or 3mg/kg/week doxorubicin. Hearts were excised under deep isoflurane anaesthesia and rapidly frozen with liquid-nitrogen cooled Wallenberger tongs. Total mRNA was extracted with a Qiagen RNeasy fibrous tissue mini kit. Gene set enrichement analysis (GSEA) shows that unlike previously reported, oxidative stress is not involved in the cardiac pathology of our model (reduced cardiac function and atrophy). However, gene sets responsible for mRNA processing, ribosomes and protein synthesis and processing are decreased in doxorubicin-treated rat hearts compared to saline control hearts.

2020-11-10 | GSE154603 | GEO

Conditioning-1

Project description:Conditioning-1

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MicroRNA profiling of the failing heart after myocardial infarction induction and doxorubicin treatment

Project description:The use of anthracycline antibiotics such as doxorubicin (DOX) has greatly improved the mortality and morbidity of cancer patients. However, the associated risk of cardiomyopathy has limited their clinical application. DOX-associated cardiotoxicity is irreversible and progresses to heart failure (HF). For this reason, a better understanding of the molecular mechanisms underlying these adverse cardiac effects is essential to develop improved regimes that include cardioprotective strategies. MicroRNAs (miRNAs) are short non-coding RNAs that are able to post-trascriptionally regulate gene expression. MiRNAs have been demonstrated to be involved in both cancer and cardiovascular disease. Therefore, we were interested in unveiling the potential role of miRNAs in chemotherapy-induced HF. We used a combination of three different models to recreate this cardiac toxicity (acute in vitro DOX treatment, DOX-induced HF in vivo and a myocardial infarction -MI- leading to failure model) to study the pattern of dysregulated miRNAs. Using RNA from all three conditions, miRNA microarray profiling was performed and a common miRNA signature was identified. Interestingly, these dysregulated miRNAs have been previously identified as involved in the failing heart. Our results suggest that DOX is able to alter the expression of miRNAs implicated in HF, in vitro as well as in vivo. The present study is a microRNA profiling of the damaged cardiac muscle (cardiomyocyte cell population), following either myocardial infarction (MI) induction or doxorubicin (DOX) treatment. Two DOX-treated models were included: ARC exposed to DOX in vitro and a validated DOX-induced heart failure model generated by repeated administration of DOX injections.

2013-01-29 | E-GEOD-36239 | biostudies-arrayexpress

Transcription profiling of rat hearts isolated perfused and exposed to doxorubicin

Project description:We used microarrays to detail transcriptional changes in the rat heart in response to doxorubicin, a chemotherapeutic drug known to induce cardiac disfunction/heart failure Experiment Overall Design: Langendorff perfusion of isolated hearts with/without doxorubicin

2009-01-14 | E-GEOD-12260 | biostudies-arrayexpress

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