Mongolian medicine Eerdun-Wurile promotes myocardial regeneration by regulating MVDA in zebrafish
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ABSTRACT:
PROVIDER: PRJNA1213724 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32060478_1.fastq.gz | Fastqsanger.gz | |||
| SRR32060478_2.fastq.gz | Fastqsanger.gz | |||
| SRR32060479_1.fastq.gz | Fastqsanger.gz | |||
| SRR32060479_2.fastq.gz | Fastqsanger.gz | |||
| SRR32060480_1.fastq.gz | Fastqsanger.gz |
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Project description:Myocardial infarction (MI) is a leading cause of death and disability worldwide. The promotion of myocardial regeneration is a promising therapeutic strategy for acute MI. Using a zebrafish ventricular ablation system, we found that the Mongolian traditional medicine Eerdun-Wurile (EW) promotes myocardial regeneration in zebrafish. EW treatment significantly accelerated proliferation of myocardial cells and improved cardiac function. Transcriptome sequencing revealed a significant decrease in mevalonate diphosphate decarboxylase a (mvda) expression in the metronidazole-induced ventricular ablation group, whereas mvda expression was restored in the EW group. mvda knockdown using morpholino oligonucleotides reversed the EW-mediated myocardial regeneration, whereas mvda overexpression enhanced the regenerative ability. In conclusion, EW may promote zebrafish myocardial regeneration, accelerate myocardial cell proliferation, and improve cardiac function by upregulating mvda expression. Our data partially revealed the molecular mechanism by which EW promotes myocardial regeneration and repair, and provides experimental data and novel insights for advancing MI treatment.
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Project description:Myocardial regeneration capacity declines during the first week after birth and is linked to the adaptation to oxidative metabolism. Utilizing this regenerative window, we characterized the metabolic changes in myocardial injury in 1-day-old regeneration-competent and 7-day-old regeneration-compromised mice. The mice were either sham-operated or received left anterior descending coronary artery ligation, to induce myocardial infarction (MI) and acute ischemic heart failure. Myocardial tissue samples were collected after 21 days for metabolomics, transcriptomics and proteomics analyses. Phenotypic characterizations were carried out using echocardiography, histology as well as mitochondrial structural and functional measurements. By integrating the findings from metabolome and transcriptome examinations, we identified mitochondrial dysfunction at the level of the carnitine shuttle contributing to myocardial regeneration incompetence. Regeneration failure was linked to accumulation of acylcarnitines and insufficient metabolic capacity for fatty acid beta-oxidation. We further identified specific transcription factors and post-transcriptional regulation contributing to both regeneration competence and failure. Rather than shifting from the preferred myocardial oxidative fuel source, our results put forward the facilitation of mitochondrial fatty acid transport and improving the beta- oxidation pathway to overcome the metabolic barriers for repair and regeneration in adult mammals after MI and heart failure.
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Project description:Myocardial regeneration capacity declines during the first week after birth and is linked to the adaptation to oxidative metabolism. Utilizing this regenerative window, we characterized the metabolic changes in myocardial injury in 1-day-old regeneration-competent and 7-day-old regeneration-compromised mice. The mice were either sham-operated or received left anterior descending coronary artery ligation, to induce myocardial infarction (MI) and acute ischemic heart failure. Myocardial tissue samples were collected after 21 days for metabolomics, transcriptomics and proteomics analyses. Phenotypic characterizations were carried out using echocardiography, histology as well as mitochondrial structural and functional measurements. By integrating the findings from metabolome and transcriptome examinations, we identified mitochondrial dysfunction at the level of the carnitine shuttle contributing to myocardial regeneration incompetence. Regeneration failure was linked to accumulation of acylcarnitines and insufficient metabolic capacity for fatty acid beta-oxidation. We further identified specific transcription factors and post-transcriptional regulation contributing to both regeneration competence and failure. Rather than shifting from the preferred myocardial oxidative fuel source, our results put forward the facilitation of mitochondrial fatty acid transport and improving the beta- oxidation pathway to overcome the metabolic barriers for repair and regeneration in adult mammals after MI and heart failure.
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Project description:Ischemic cardiopathy is the leading cause of death in the world, for which efficient regenerative therapy is not currently available. In mammals, after a myocardial infarction episode, the damaged myocardium is replaced by scar tissue featuring collagen deposition and tissue remodelling with negligible cardiomyocyte proliferation. Zebrafish, in contrast, display an extensive regenerative capacity as they are able to restore completely lost cardiac tissue after partial ventricular amputation. Due to the lack of genetic lineage tracing evidence, it is not yet clear if new cardiomyocytes arise from existing contractile cells or from an uncharacterised set of progenitors cells. Nonetheless, several genes and molecules have been shown to participate in this process, some of them being cardiomyocyte mitogens in vitro. Though questions as what are the early signals that drive the regenerative response and what is the relative role of each cardiac cell in this process still need to be answered, the zebrafish is emerging as a very valuable tool to understand heart regeneration and devise strategies that may be of potential value to treat human cardiac disease. Here, we performed a genome-wide transcriptome profile analysis focusing on the early time points of zebrafish heart regeneration and compared our results with those of previously published data. Our analyses confirmed the differential expression of several transcripts, and identified additional genes the expression of which is differentially regulated during zebrafish heart regeneration. We validated the microarray data by conventional and/or quantitative RT-PCR. For a subset of these genes, their expression pattern was analyzed by in situ hybridization and shown to be upregulated in the regenerating area of the heart. The specific role of these new transcripts during zebrafish heart regeneration was further investigated ex vivo using primary cultures of zebrafish cardiomyocytes and/or epicardial cells. Our results offer new insights into the biology of heart regeneration in the zebrafish and, together with future experiments in mammals, may be of potential interest for clinical applications. In order to study zebrafish heart regeneration, a time course experiment was realized where amputated heart regenerating were compared to control heart. Samples in triplicate were extracted at 1, 3, 5 and 7 days post-amputation.
2010-03-09 | E-GEOD-17993 | biostudies-arrayexpress
Project description:Conditional expression of dominant-negative HIF1a in zebrafish cardiomyocytes severely inhibits heart regeneration. To understand more about the mechanism, we performed microarray analysis of wildtype regenerating zebrafish and dnHIF1a regenerating zebrafish to determine which genes are regulated by hypoxia/HIF1a.
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Project description:Unlike human hearts, zebrafish hearts efficiently regenerate after injury. Regeneration is driven by the strong proliferation response of its cardiomyocytes to injury. In this study, we show that active telomerase is required for cardiomyocyte proliferation and full organ recovery, supporting the potential of telomerase therapy as a means of stimulating cell proliferation upon myocardial infarction. Heart transcriptomes of WT and telomerase defective adult zebrafish animals were profiled by RNASeq, in control conditions and 3 days after heart cryoinjury.
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Project description:Pre-existent adult sox10+ cardiomyocytes contribute to myocardial regeneration in the zebrafish
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Project description:The myocardial tissues of the ischemic left ventricle and the peri-ischemic rim (an approximately 1 mm rim of normal-appearing tissues) were removed, and the remaining tissues that consisted of non-ischemic left ventricle were obtained for the transcriptional analysis. The total RNA was extracted from the myocardia from the sham (n = 3), myocardial ischemia model (n = 3), and a traditional Chinese medicine formula treated on myocardial ischemia (n = 3) groups. Beads that contained oligo were used to isolate the poly mRNA from the total RNA and then the rRNA was subsequently removed. The amplified library was sequenced on a HiSeq 2500 sequencing machine (Illumina, San Diego, California, USA) with a 50 bp SE strategy. Using CASAVA software, the images generated by the Illumina sequencers were converted into raw reads by base-calling.
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