Potential cardiac-derived exosomal miRNAs involved in cardiac healing and remodeling after myocardial ischemia-reperfusion injury
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ABSTRACT:
PROVIDER: PRJNA1066882 | ENA |
REPOSITORIES: ENA
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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
Project description:This RNA-sequencing was performed to determine the differentially expressed mRNA after inhibition of Hmbox1 in cardiac ischemia/reperfusion injury
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Project description:Primary cardiac myocytes isolated from neonatal Wistar rats were cultured and simulated ischemia/reperfusion injury were conducted on them in the presence or absence of decorin. Decorin is a small leucin-rich proteoglycan, which has a cardiocytoprotective effect. The underlaying mechanism of this cardiocytoprotective phenomenon is unknown, therefore our aim was to investigate the changes in the mRNA expression between the decorin (3nM) treated and vehicle-treated control cells.
2020-12-31 | E-MTAB-9325 | biostudies-arrayexpress
Project description:Data used in the publication: Analysis of cardiac ischemia-reperfusion injury using DIA proteomics and N-terminomics reveals alterations in mitochondrial function and metabolism
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Project description:The objective of this study was to test how restoration of mitochondrial respiration using AOX affects the development of cardiac ischemia-reperfusion (IR) injuries in C57BL/ 6J mice. AOX transgenic mice have Ciona intestinalis AOX coding sequence knocked into the Rosa26 locus with AOX expression controlled by a CAG promoter as described elsewhere (Szibor et al. (2017) Dis Model Mech 10: 163–171). Consequences of 45 min of cardiac ischemia were studied 3 and 9 weeks after reperfusion in both wild-type and AOX litter mates.
2020-01-30 | PXD014061 | Pride
Project description:This study was a part of a larger study assessing the response of young pigs to cardiac ischemia/reperfusion (IR) injury. A mild cardiac injury approach (IR) was used in post-weaned pigs (1-month), to assess regenerative repair in young large mammals after transient ischemic injury. Female and male postnatal day (P)30 pigs were subjected to cardiac ischemia (1-hour) by occlusion of the left anterior descending artery followed by reperfusion (IR), or to sham operation. In pigs subjected to IR, myocardial damage occurred, indicated by increased circulating cardiac troponin I 2-hours post-ischemia. In addition, cardiac ejection fraction (EF) was significantly decreased 2-hours post-ischemia and reduced EF was maintained to the 4-week study end-point. Histology demonstrated evidence of CM cell cycling at 2-months of age in multinucleated CMs in both sham-operated and IR pigs. Following IR, regional scar formation and inflammation in the epicardial region proximal to injury were observed 4-weeks post-IR. Sex differences in cardiac function and collagen deposition were found, highlighting the importance of representing both sexes in cardiac injury studies. Together, our results describe an effective novel cardiac injury model in 1-month old swine, at a time when CM are still cycling. However, pigs subjected to IR show a prolonged decrease in cardiac function, and the formation of a small, regional scar with increased inflammation. Together, these data demonstrate that 1-month old pigs do not regenerate myocardium, but form a scar, after transient IR injury.
2020-04-27 | GSE137293 | GEO
Project description:Decorin protects cardiac myocytes against simulated ischemia/reperfusion injury
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Project description:Role of reducing Hmbox1 in cardiac ischemia/reperfusion injury
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Project description:Mice were exposed to cardiac ischemia/reperfusion injury and sacrificed after 1 or 4 days. Hearts were stained with Evans blu/TTC to isolate the at risk area. Hearts were divided into 1mm slices, the at risk area of any slice were pooled together before RNA extraction. Mice were divided into 3 different groups: Sham animals have been subjected to the surgical procedure without the induction of the ischemia and reperfusion injury and represent the control animals; LAD group is represented by animals subjected to the surgical procedure and the induction of the ischemia and reperfusion imjury; MLAD group is represented by animals subjected to the surgical procedure and the induction of the ischemia and reperfusion injury, followed by myriocin treatment (SLN/Myr) at the beginning of reperfusion.
2019-07-07 | GSE133913 | GEO
Project description:Calpain 1 and 2 (CPN1/2) are calcium-dependent cysteine proteases that exist in cytosol and mitochondria. Pharmacologic inhibition of CPN1/2 decreases cardiac injury during ischemia (ISC) – reperfusion (REP) by improving mitochondrial function. However, the protein targets of CPN1/2 activation during ISC-REP are unclear. CPN1/2 include a large subunit and a small regulatory subunit 1 (CPNS1). Genetic deletion of the CPNS1 eliminates the activities of both CPN1 and CPN2. Conditional, cardiomyocyte specific CPNS1 knockout (KO) mice were used in the present study to clarify the role of CPN1/2 activation in mitochondrial damage during ISC-REP with an emphasis on identifying the potential protein targets of CPN1/2. Isolated hearts from wild type (WT) or CPNS1 KO mice underwent 25 min in vitro global ISC and 30 min REP. LDH activity in coronary effluent was measured to reflect cardiac injury. Mitochondria were isolated from the hearts. Cardiac injury was decreased in CPNS1 KO mice following ISC-REP compared to WT. ISC-REP decreased the rate of oxidative phosphorylation in WT but not in CPNS1 KO mice when glutamate + malate was used as complex I substrate. KO of CPNS1 led to a smaller decrease in CRC (calcium retention capacity) following REP compared to WT. The H2O2 generation was decreased in KO mitochondria following ISC-REP compared to WT. KO of CPNS1 also resulted in less cytochrome c release from mitochondria. Proteomic analysis of the isolated mitochondria showed that KO of CPNS1 increased the abundance of ribosomal proteins and mitochondrial biogenesis proteins. These results show that activation of CPN1/2 increases cardiac injury during ischemia-reperfusion by damaging mitochondria.
2021-12-21 | PXD022689 | Pride