Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mechanism for Cortical Bone Stem Cell-Derived Exosomes' Therapeutic Effect on Myocardial Ischema Reperfusion and Remodeling

ABSTRACT: Mechanism for Cortical Bone Stem Cell-Derived Exosomes' Therapeutic Effect on Myocardial Ischema Reperfusion and Remodeling

PROVIDER: PRJNA730036 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14551700.fastq.gz	Fastqsanger.gz
	SRR14551701.fastq.gz	Fastqsanger.gz
	SRR14551702.fastq.gz	Fastqsanger.gz
	SRR14551703.fastq.gz	Fastqsanger.gz
	SRR14551704.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 128

Similar Datasets

Mesenchymal Stromal Cell-Derived Exosomes Attenuate Myocardial Ischemia-Reperfusion Injury through miR-182-Regulated Macrophage Polarization

Project description:Aims: Mesenchymal stem cells (MSCs) gradually become attractive candidates for cardiac inflammation modulation, yet understanding of the mechanism remains elusive. Strikingly, recent studies indicated that exosomes secreted by MSCs might be a novel mechanism for the beneficial effect of MSCs transplantation after myocardial infarction. We therefore explored the role of MSC-derived exosomes (MSC-Exo) in the immunomodulation of macrophages after myocardial ischemia-reperfusion and its implications in cardiac injury repair. Methods and Results: Exosomes were isolated from the supernatant of MSCs using a gradient centrifugation method. Administration of MSC-Exo through intramyocardial injection after myocardial ischemia reperfusion reduced infarct size and alleviated inflammation level in heart and serum. Systemic depletion of macrophages with clodronate liposomes abolished the curative effects of MSC-Exo. MSC-Exo modified the polarization of M1 macrophages to M2 macrophages both in vivo and in vitro. miRNA-sequencing of MSC-Exo and bioinformatics analysis implicated miR-182 as a potent candidate mediator of macrophage polarization and TLR4 as a downstream target. Diminishing miR-182 in MSC-Exo partially attenuated its modulation of macrophage polarization. Likewise, knock down of TLR4 also conferred cardioprotective efficacy and reduced inflammation level in a mouse model of myocardial ischemia/reperfusion. Conclusion: Our data indicates that MSC-Exo attenuates myocardial ischemia/reperfusion injury via shuttling miR-182 that modifies the polarization state of macrophages. This study sheds new light on the application of MSC-Exo a potential therapeutic tool for myocardial ischemia/reperfusion injury.

2021-09-01 | GSE120149 | GEO

Mechanism for Cortical Bone Stem Cell-Derived Exosomes' Therapeutic Effect on Myocardial Ischema Reperfusion and Remodeling

Project description:The goal of this study was to understand the effect of human cortical bone stem cells on human cardiac fibroblast activation. We treated normal human cardiac fibroblasts +/- 50 ng/mL TGFBeta +/- 2,000,000 human cortical bone stem cell-derived exosome particles per fibroblast treated for 72 hours and then isolated RNA for RNA-sequencing.

2022-02-02 | GSE174490 | GEO

Potential cardiac-derived exosomal miRNAs involved in cardiac healing and remodeling after myocardial ischemia-reperfusion injury

Project description:Migratory cells exist in the heart, such as immune cells, fibroblasts, endothelial cells, etc. During my-ocardium injury, such as ischemia-reperfusion (MIRI), cells migrate to the site of injury to perform repair functions. However, excessive aggregation of these cells may exacerbate damage to the structure and function of the heart, such as acute myocarditis and myocardial fibrosis. Myocardial injury releases exosomes, which are a type of vesicle with signal transduction function and the miRNA carried by exosomes can control cell migration function. Therefore, regulating this migratory cell population through cardiac-derived exosomal miRNA is crucial for protecting and maintaining cardiac function. Through whole transcriptome RNA sequencing, exosomal miRNA sequencing and single-cell dataset analysis, we (1) determined the potential molecular regulatory role of the lncRNA‒miRNA‒mRNA axis and an important lncRNA (MSTRG.91411.6) in MIRI, (2) screened four important exosomal miRNAs that could be released by cardiac tissue, and (3) screened seven genes related to cell locomo-tion that are regulated by four miRNAs, among which Tradd and Ephb6 may be specific for promoting migration of different cells of myocardial tissue in myocardial infarct. We generated a core miRNA‒mRNA network based on the functions of the target genes, which may be not only a target for cardiac repair but also a potential diagnostic marker for interactions between the heart and other tissues or or-gans. In conclusion, we elucidated the potential mechanism of MIRI in cardiac remodeling from the perspective of cell migration, and inhibition of cellular overmigration based on this network may pro-vide new therapeutic targets for MIRI and to prevent MIRI from developing into other diseases.

2024-10-23 | GSE253760 | GEO

Vitamin B12 alleviates myocardial ischemia/reperfusion injury

Project description:To examine the protective effect of B12 on myocardial ischemia/reperfusion injury and figure out the mechanism of B12.

2024-01-01 | GSE225105 | GEO

Ckmt2 for Evaluating Reperfusion Injury in Acute Myocardial Infarction

Project description:Mitochondrial Creatine Kinase 2 (Ckmt2) as a Plasma-Based Biomarker for Evaluating Reperfusion Injury in Acute Myocardial Infarction

2024-10-17 | PXD055738 | Pride

CircRNA expression profile analysis of myocardial reperfusion injury in rats

Project description:To explore the differences in the expression of circRNA in myocardial ischemia-reperfusion injury and the potential effects of these differences in circRNA. Methods 6 SPF male SD rats were randomly divided into two groups, including 3 in Myocardial ischemia reperfusion group and 3 threading without ligation in control group by ligating the left anteriors branch for 40 minutes and reperfusing for 2 hours to establish a model of myocardial ischemia reperfusion injury. The myocardial specimens from the infarct area were taken for high-throughput sequencing analysis to obtain differently expressed circRNA. After that, GO and KEGG analysis were performed to speculate on the biological functions and possible biological pathways involved. RT-qPCR was used to verify the sequencing results of differential circRNA, and bioinformatics analysis predicted that circRNA could combine with miRNA to construct a visual network diagram and their interaction. Results Analyzing of 13576 circRNAs detected in 6 rats from MIRI group and control group, A total of 132 circRNAs showed significant differential expression, of which 82 were up-regulated and 50 were down-regulated. The results of GO and KEGG analysis suggest that differential circRNA is closely related to myocardial ischemia reperfusion injury, and KEGG analysis suggests that differential circRNA is involved in calcium, AMPK, mTOR and adrenaline signal pathways. 4 circRNAs were extracted from the up-regulated circRNA for RT-qPCR verification, and the results of 2 were consistent with the high-throughput sequencing results. circRNA-miRNA interaction analysis shows that circRNA interacts with a variety of miRNAs. Conclusions The expression of circRNA in myocardial reperfusion injury rats is significantly different, which may be involved in the occurrence and development of myocardial ischemia-reperfusion injury through miRNA sponge action of circRNA.

2022-06-30 | GSE207093 | GEO

Vitamin B12 alleviates myocardial ischemia/reperfusion injury

Project description:Vitamin B12 alleviates myocardial ischemia/reperfusion injury

| PRJNA933927 | ENA

Mesenchymal Stromal Cell-Derived Exosomes Attenuate Myocardial Ischemia-Reperfusion Injury through miR-182-Regulated Macrophage Polarization

Project description:Mesenchymal Stromal Cell-Derived Exosomes Attenuate Myocardial Ischemia-Reperfusion Injury through miR-182-Regulated Macrophage Polarization

| PRJNA491732 | ENA

CaM Kinase II mediates maladaptive post-infarct remodeling but not acute myocardial ischemia/reperfusion injury

Project description:Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. CaMKIIÎ´C was up-regulated already one day after I/R injury but surprisingly, acute I/R injury was neither affected in CaMKIIÎ´-deficient mice, CaMKIIÎ´-deficient mice in which the splice variants CaMKIIÎ´B and C were re-expressed nor in conditional CaMKIIÎ´/Î³ double-knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfunction. Leukocyte infiltration was not altered one day but five days after I/R, explaining the late effects of CaMKII deletion on post-I/R remodeling. Other than reported before, we demonstrate that CaMKII is not critically involved in the immediate mechanisms that regulate acute I/R injury but in the process of post-infarct remodeling. We analysed 6 groups in total: 3 groups from wild-type control animals and 3 groups from CaMKII delta/gamma double-KO mice. Sham operated animals served as controls in both wild-type and KO animal groups. 2 different time points in ischia/reperfusion operated animals were investigated: 1 day and 5 days post-surgery.

2014-09-08 | E-GEOD-58486 | biostudies-arrayexpress

Hif2a-cardiomyocyte deficient mice response to myocardial ischemia and reperfusion

Project description:Analysis of heart of Hypoxia-inducible 2 alpha-deficient mice, specific in cardiomyocytes (Hif2aloxP/loxP Myosin Cre+) subjected to myocardial ishcemia reperfusion. Hif2a belongs to the family of transcription factors, that regulate a transcriptional response to tissue hypoxia.

2016-12-31 | GSE67308 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data