Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA355652 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparison of both LncRNAs and mRNAs expression in the border zone of the myocardial infarction rats and the sham operation rats Border zone (BZ) of the myocardial infarction is critical to patients. Current treatments of myocardial infarction are primarily aimed to save the dying myocardial cell in the border zone. During myocardial infarction, certain changes in BZ, e.g, apoptosis, fibrosis, inflammation, etc, played an important role in deciding the survival. Impairment and recovery of BZ has been linked to gene expression changes. The aim of our study was to obtain a global expression profile of lncRNAs and mRNAs of the border zone in Wistar rats myocardial infarction, and identify the changes during myocardial infarction.
2016-12-02 | GSE90745 | GEO
Project description:Very little information is available about non-coding(nc)RNAs and their role in regulating tissue responses in myocardial ischemia and acute infarction. We measured for the first time nascent RNA transcription of protein coding genes, primary(pri)-miRNAs, long non-coding(lnc)RNAs and enhancer(e)RNAs in healthy myocardium, border zone to ischemia and infarction area in pig hearts using GRO-seq. The gene expression analysis indicated a gradient of induction of inflammatory mediators, and repression of PPAR-signaling and oxidative phosphorylation. An exception to rule was A1 adenosine receptor, which exhibited induced gene expression in the border zone, where it might increase myocardial resistance to ischemia, but repression in the ischemic zone. In addition, we interrogated for the first time the transcriptional regulation of pri-miRs and provide evidence that several arrhythmia-related target genes are further repressed at post-transcriptional level. We identified 450 lncRNAs which were differently regulated by ischemia including novel lncRNAs expressed in antisense orientation to major myocardial transcription factors GATA4, GATA6 and KLF6. Finally, characterization of enhancers exhibiting differential expression of eRNAs, pointed a central role for KLF, MEF2C, ETS, NFY, ATF, E2F2 and NRF1 transcription factors in determining tissue-specific responses to ischemic insult. In conclusion, GRO-Seq allowed us to follow the gradient of gene expression occurring in the ischemic heart and identify novel ncRNAs regulated by oxygen deprivation. These findings have identified potential new targets for diagnosis and treatment of myocardial ischemia based on acute changes in eRNA, lncRNA and miRNA expression in the affected heart.
2017-06-19 | GSE81155 | GEO
Project description:Affymetrix microarray analysis of molecular changes after myocardial infarction. Samples of heart tissue were analyzed after myocardial infarction from WT and reg3beta knock-out mice. Samples from scar tissue and samples adjacent to the scar were analyzed. In the experiment we primarily compared infarction zone of wild-type to infarction zone of knock-out animals, and remote zone of wild-type to remote zone of knock-outs.
2015-06-29 | E-MTAB-2561 | biostudies-arrayexpress
Project description:Regulation of gene expression with thyorid hormone in rats with myocardial infarction
| PRJNA150923 | ENA
Project description:Myocardial infarction causes a massive loss of cardiomyocytes, leading to the formation of a fibrotic scar resulting in impaired cardiac function. In contrast to mammals, zebrafish display robust cardiac regeneration following injury due to the proliferation of pre-existing cardiomyocytes in the injury border zone. Here, we aim to identify transcriptomic differences that will help explain the differential cardiac regenerative capacity observed between the injured zebrafish and mammalian heart. First, we transcriptionally profiled the border zone of the injured mouse heart, which does not support regeneration. Then, we bioinformatically compared the transcriptome of the mouse border zone with the zebrafish border zone, identifying many genes and processes overlapping or diverging between the two species. Interestingly, we identified the architectural chromatin remodeller hmga1a to be expressed in the zebrafish, but not the mouse border zone. Using a loss-of-function hmga1a mutant we show that hmga1a is required for border zone cardiomyocyte proliferation and zebrafish heart regeneration. Using single-cell RNA-sequencing, we identify the near absence of proliferative cardiomyocyte sub-populations in hmga1a mutant border zones. Furthermore, we show that overexpression of hmga1a can induce cardiomyocyte proliferation in uninjured zebrafish hearts. Using a combination of RNA- and ATAC-sequencing, we show that hmga1a overexpression leads to the induction of a broad border zone-like gene program, including robust chromatin remodelling. Last, we provide evidence suggesting that overexpression of Hmga1 can stimulate mammalian cardiomyocyte proliferation and functional recovery post myocardial infarction. Taken together, through transcriptional comparison of the zebrafish and mouse border zone we have identified hmga1a as a key determinator of cardiac regenerative potential.
2025-01-01 | GSE164729 | GEO
Project description:Transcriptional profiling of left ventricle and peripheral blood cells in rats with post-myocardial infarction
| PRJNA205867 | ENA
Project description:miRNA Expression Profile and Effect of Wenxin Granule in Rats with Ligation-Induced Myocardial Infarction
| PRJNA378605 | ENA
Project description:In contrast to mammals, zebrafish regenerate heart injuries via proliferation of cardiomyocytes located at the wound border. Here, we show that tomo-seq can be used to identify whole-genome transcriptional profiles of the injury zone, the border zone and the healthy myocardium. Interestingly, the border zone is characterized by the re-expression of embryonic cardiac genes that are also activated after myocardial infarction in mouse and human, including targets of Bone Morphogenetic Protein (BMP) signaling. Endogenous BMP signaling has been reported to be detrimental to mammalian cardiac repair. In contrast, we find that genetic or chemical inhibition of BMP signaling in zebrafish reduces cardiomyocyte dedifferentiation and proliferation, ultimately compromising myocardial regeneration, while bmp2b overexpression is sufficient to enhance it. Our results provide a resource for further studies on the molecular regulation of cardiac regeneration and reveal intriguing differential cellular responses of cardiomyocytes to a conserved signaling pathway in regenerative versus non-regenerative hearts. To generate spatially-resolved RNA-seq data for injured zebrafish hearts (3 and 7 days-post-injury), we cryosectioned samples, extracted RNA from the individual sections, and amplified and barcoded mRNA using the CEL-seq protocol (Hashimshony et al., Cell Reports, 2012) with a few modifications. Libraries were sequenced on Illumina NextSeq using 75bp paired end sequencing.
2016-01-11 | E-GEOD-74652 | biostudies-arrayexpress
Project description:MicroRNAs are important cellular components and their dysfunctions are associated with various disease. Acute myocardial infarction (AMI) is one of the most serious cardiovascular diseases. Although several miRNAs have been reported to be associated with AMI, more novel miRNAs are needed to be investigated to ascertain if they are associated with AMI. SD rats (180-200g) was divided into sham-control group and two days group after AMI, seven days group after AMI, fourteen days group after AMI, each group has six individual animals total RNA was taken from the border-zone myocardium , low molecular weight RNA was seperate and labeled , and then hybridized to capitalbio V2 biochip representing about 924 microRNA . three chip were test in each group, and the procedure was repeated twice.
2010-04-22 | E-GEOD-19695 | biostudies-arrayexpress
Project description:Endothelial cells were isolated from the infarct region (anteroapical wall distal to the coronary artery ligation site representing the infarct core and border zone) 3 days after sham or acute myocardial infarction (AMI) surgery. AMI was induced by 60 min coronary ligation followed by reperfusion. Endothelial cells were subjected to single cell RNA sequencing.
2022-06-20 | GSE198401 | GEO