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.
2025-06-16 | GSE287547 | GEO
Project description:Objective: Detection and analysis of Mongolian medicine Narenmandula the kernel full of adriamycin nephrosis rats kidney tissue expression of miRNA. Methods: The biological information of the differentially expressed miRNA between the normal group, the model group and the Mongolian medicine Narenmandula group was studied by Affymetrix miRNA chip detection. Results: The biological information of miRNA expression in kidney tissues of rats with doxorubicin nephropathy was analyzed by detection, which laid a foundation for further elucidating the multi-target regulatory role of Mongolian medicine Narenmandula in renal function protection and provided data. The biological information of miRNA expression in renal tissues of doxorubicin rats was detected and analyzed using Affymetrix miRNA chip detection technology, which laid a foundation for further elucidating the multi-target regulation effect of the renal function protection and provided data of Mongolian medicine Narenmandula .
2019-12-14 | GSE123776 | GEO
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.
2022-02-04 | MSV000088783 | GNPS
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.
2022-02-04 | MSV000088783 | MassIVE
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. We amputated both wildtype and dnHIF1a zebrafish and allowed them to regenerate for 7 days, then compared their transcriptomic profile with unamputated wildtype and dnHIF1a zebrafish, respectively.
2013-01-15 | E-GEOD-39842 | biostudies-arrayexpress
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.
2013-01-15 | GSE39842 | GEO
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.
2015-08-06 | E-GEOD-71755 | biostudies-arrayexpress
Project description:<p>Abstract</p><p>Objective: Wulanwendusu-11 (WLWDS-11), a traditional Mongolian medicinal formula, is commonly used for the treatment of Cardiovascular diseases. However, its therapeutic material basis and in vivo metabolic profile in the context of chronic myocardial ischemia-reperfusion injury (MIRI) remain to be elucidated.</p><p>Methods: C57BL/6J mice were randomized into six experimental groups: MIRI model, sham surgery, and treatment groups for compound Danshen dripping pills (CDDP) plus three dosages of WLWDS-11 (denoted WLWDS-11-L, WLWDS-11-M, and WLWDS-11-H). General physiological indicators of mice in each group were observed, body weight, myocardial structure and pathological features were assessed by electrocardiogram, plasma cardiac enzyme levels. Immunohistochemical staining was used to detect the pathological changes in the heart. Immunofluorescence assay was used to detect the degree of apoptosis. qRT-PCR and Western blot were used to detect the expression of COX4I1, NDUFB8, SDHA, TFAM, RIPK1, RIPK3, MLKL and TNF-α. Metabolomics and metagenomics were used to analyze treatment effects on intestinal microbiota and metabolites.</p><p>Results: WLWDS-11 (especially in high dose) can significantly improve the cardiac function, reduce the area of myocardial infarction and weaken apoptosis and fibrosis in MIRI mice. Metabolomic profiling identified 1,632 qualitative secondary metabolites, 13 annotated secondary metabolites, 125 annotated tertiary metabolites, and 296 annotated quaternary metabolites. The top 10 differential metabolites included lysophosphatidylinositol (LPI) 18:2, phlorobenzophenone, LPI 20:4, and 2-arachidonoyl-1-stearoyl-sn-glycero-3-phosphoethanolamine. Pathway screening was conducted to identify the key pathways most closely associated with metabolic differences, which included arginine and proline metabolism, biosynthesis of unsaturated fatty acids, and phenylalanine, tyrosine, and tryptophan biosynthesis. </p><p>Metagenomic results showed that the sham and WLWDS-11-H groups were enriched for the RNA polymerase (KEGG pathway identifier: ko03020), alanine, aspartic acid, and glutamate metabolism (ko00250), and aminoacyl-tRNA biosynthesis (ko00970) pathways. Correlation hierarchical cluster analysis of differential flora and metabolites showed that Kosakonia, Constantimarinum, and Syncephalis genera were associated with the metabolites 1-myristoyl-sn-glycero-3-phosphocholine and batatasin III, and had a strong correlation with 1-O-hexadecyl-sn-glycero-3-phosphocholine. At the species level, three Helicobacter spp. were strongly associated with metabolites such as perfluorobutanoic acid, Ile-Leu, Leu-Ile, and nanaomycin E. Multiomics integration analysis showed that MIRI caused intestinal flora imbalance (such as Prevost enrichment) and serum metabolism disorder (such as accumulation of oxidized lipids and lysophospholipids, arginine/proline and unsaturated fatty acid metabolism disorder). The intervention of WLWDS-11 effectively reshaped the intestinal microbial community and made the metabolic spectrum return to normal. Correlation and network analysis confirmed the correlation between specific intestinal bacteria (such as Prevost, Kosakonia and Helicobacter) and host metabolites, and formed a flora-metabolite axis regulated by WLWDS-11. KEGG pathway analysis further confirmed the effects of the treatment on key pathways, including necrotizing apoptosis and oxidative phosphorylation. From the point of view of mechanism, WLWDS-11 reversed the mitochondrial dysfunction induced by MIRI by up-regulating the expressions of COX4I 1, NDUFB8, SDHA and TFAM. By inhibiting the RIPK 1/RIPK 3/MLKL pathway and TNF-α, necrotizing apoptosis and inflammatory response are inhibited. These results suggest that WLWDS-11 may protect MIRI's heart by regulating the metabolic pathway of flora. These findings identify WLWDS-11 as a potential candidate drug and provide a molecular mechanistic basis for the clinical treatment of MIRI. Conclusion: WLWDS-11 positively reshaped the gut microbial environment by suppressing pathogenic bacteria and promoting beneficial strains, thereby fostering eubiosis, attenuating cardiac pathology, and ultimately conferring cardioprotection.</p>
2025-11-22 | MTBLS13370 | MetaboLights
Project description:Pre-existent adult sox10+ cardiomyocytes contribute to myocardial regeneration in the zebrafish
| PRJNA551951 | ENA