Diagnostic value of circulating miR-146b-5p and miR-222-5p in patients with acute myocardial infarction
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE239822 | GEO | 2024/08/01
REPOSITORIES: GEO
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Project description:Diagnostic value of circulating miR-146b-5p and miR-222-5p in patients with acute myocardial infarction
| PRJNA1001022 | ENA
Project description:Rationale and Objectives: Cellular therapies are hampered by poor survival and growth of grafts. We recently showed that the survival and repairing capacity of transplanted adult cells may be improved by co-expression of the anti-senescence telomerase reverse transcriptase (TERT) and anti-apoptotic myocardin (MYOCD). The current study aimed at testing whether forced co-expression of TERT and MYOCD improves post-infarct revascularization and tissue repair by adipose tissue-derived mesenchymal stromal cells (AT-MSCs). Methods: We transplanted AT-MSCs engineered to overexpress MYOCD and TERT in a murine model of acute myocardial infarction (AMI). We analyzed the immunoregulatory properties of AT-MSCs on post-AMI. We characterized in vitro and in vivo paracrine effects of AT-MSCs and their interactions with murine cardiospheres (CSps), all as parts of their reparative repertoire. Results: When transplanted into infarcted hearts of C57BL/6 mice, “rejuvenated” AT-MSCs overexpressing TERT and MYOCD (rAT-MSCs) decreased fibrosis and the intrafibrotic CD3 and B220 lymphocyte infiltration, and increased arteriolar density as well as ejection fraction compared with saline or mock-transduced AT-MSCs. These effects were accompanied by increased numbers of Ki-67+ and CD117+ cells, and the expression of cardiac actin and β-myosin heavy chain within the infarcted hearts. Both rAT-MSCs and their conditioned medium (CM) stimulated intracellular Ca2+ flux in CSps. CSp-derived cells had increased survival when preconditioned with CM or exosome-enriched fraction (Exo+) from rAT-MSCs and then exposed to simulated ischemia/reperfusion. Proteomic analysis of rAT-MSCs-Exo+ predicted the activation of vascular development and the inhibition of immune cell trafficking. Elevated concentration of miR-320a, miR-150-5p and miR-126-3p associated with regulation of apoptosis and vasculogenesis was confirmed in rAT-MSCs-Exo+. Conclusions: rAT-MSCs promote vasculogenesis and cell survival and reduce post-AMI inflammatory responses in a murine model of AMI. An integrated experimental and computational analysis revealed that Exo+ is the active component of the paracrine secretion by rAT-MSCs, with pro-angiogenic and pro-survival activities.
2020-12-02 | PXD017413 | Pride
Project description:Acute myocardial infarction (AMI) induces blood leukocytosis, which correlates inversely with patient survival. The molecular mechanisms leading to leukocytosis, and recruitment to the infarcted heart, remain poorly understood. Using an AMI mouse model, gasdermin D (GSDMD) was identified in activated neutrophils early in AMI. We demonstrated that GSDMD is required for enhanced recruitment of neutrophils and monocytes to the infarcted heart. Loss of GSDMD resulted in reduced release of IL-1β from neutrophils and reduced recruitment of neutrophils and monocytes to the infarcted heart. Knockout of GSDMD in mice significantly reduced infarct size, improved cardiac function and increased survival post AMI. Through a series of bone marrow transplantation studies and leukocytes depletion experiments, we further demonstrated that excessive bone marrow derived and GSDMD-dependent neutrophil recruitment, contributes to the detrimental immunopathology after AMI. Pharmacological inhibition of GSDMD also conferred cardioprotection post AMI, through reduction of scar size and enhancement of heart function. Our study provides new mechanistic insights into molecular regulation of neutrophil generation and recruitment after AMI, and supports GSDMD as a new target for improved ventricular remodeling and reduced heart failure after AMI.
2022-01-05 | GSE181872 | GEO
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.
2010-01-05 | GSE19695 | GEO
Project description:This study demonstrated that there were a number of dysregulated circRNAs in exosomes from OSA with AMI patients, which might be effectively served as a promising diagnostic biomarker and therapeutic targets. Objectives: Circular RNAs (circRNAs) are recently identified as a class of non-coding RNAs that participate in the incidence of acute myocardial infarction(AMI)
2022-02-23 | GSE197137 | GEO
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:Increasing evidence highlights the multiple roles of microRNAs (miRs) in the tumorigenesis of colorectal cancer (CRC); however, the molecular mechanism, particularly the target of miR-146b-5p in CRC has not been fully elucidated. The present study aimed to elucidate the influence of miR-146b-5p via regulating tumor necrosis factor receptor-associated factor 6 (TRAF6) in CRC. The expression levels of miR-146b-5p and TRAF6 in CRC tissue and cells were determined by reverse transcription quantitative PCR and western blotting. Binding between miR-146b-5p and TRAF6 was examined using a dual luciferase reporter gene assay. The impact of miR-146b-5p and TRAF6 on proliferation and migration of CRC cells was determined using Cell Counting Kit-8 and Transwell assays, respectively. An animal model of CRC was established to determine the carcinogenic effect of the miR-146b-5p-TRAF6 axis. The results demonstrated that miR-146b-5p was highly expressed in CRC tissue samples compared with in normal adjacent tissue samples and in CRC cells compared with in the normal NCM460 cell line, whereas TRAF6 was expressed at low levels. Overexpression of miR-146b-5p decreased TRAF6 expression in CRC HT29 and SW620 cells. miR-146b-5p targeted and inhibited TRAF6 expression in CRC cells. Furthermore, transfection with a miR-146b-5p mimic promoted the proliferation, migration and invasion of CRC cells and tumor growth; however, these effects were abolished by TRAF6 overexpression. Transfection with a miR-146b-5p inhibitor suppressed the proliferation of CRC cells. Taken together, the results from the present study demonstrated that miR-146b-5p could enhance the initiation and tumorigenesis of CRC by targeting TRAF6. These results will help elucidate the mechanisms underlying CRC development and will facilitate the development of targeted therapy for CRC.
| S-EPMC8815033 | biostudies-literature
Project description:Background: In spite of modern reperfusion therapies, morbidity and mortality of heart failure (HF) post myocardial infarction (MI) remain elevated. The aim of this study was to identify potential long non-coding RNAs (lncRNAs) and mRNAs in progression from acute myocardial infarction (AMI) to myocardial fibrosis (MF) to HF. Methods: Firstly, blood samples from 3 AMI patients, 3 MF patients and 3 HF patients were used for RNA sequencing. Secondly, differentially expressed lncRNAs and mRNAs were obtained in MF vs AMI and HF vs MF, followed by functional annotation of common differentially expressed mRNAs between two groups. Thirdly, interaction networks of lncRNA-nearby targeted mRNA and lncRNA-co-expressed mRNA were constructed in MF vs AMI and HF vs MF. Finally, expression validation and diagnostic capability analysis of selected lncRNAs and mRNAs were performed. Results: Several lncRNA-co-expressed/nearby targeted mRNAs pairs including AC005392.3/AC007278.2-IL18R1, AL356356.1/AL137145.2-PFKFB3 and MKNK1-AS1/LINC01127-IL1R2 were identified. Several signaling pathways including TNF signaling pathway and cytokine-cytokine receptor interaction (involved IL18R1), fructose and mannose metabolism and HIF-1 signaling pathway (involved PFKFB3), hematopoietic cell lineage and fluid shear stress and atherosclerosis (involved IL1R2) and estrogen signaling pathway (involved FKBP5) were screened out. FKBP5, IL1R2, IRAK3, LRG1, RNASE1 and PLAC4 had a potential diagnostic value for HF.
2021-07-13 | GSE168281 | GEO
Project description:Duck Tembusu virus (DTMUV), belonging to the Flaviviridae family, is a major virus that affects duck health in China. MicroRNAs (miRNAs) play an important role in viral replication. However, little is known about the function of miRNAs during DTMUV infection. Here, the host miR-146b-5p was found to regulate DTMUV replication. When DTMUV infected duck embryo fibroblasts (DEFs), the expression levels of miR-146b-5p increased significantly over time. Moreover, the viral RNA copies, E protein expression levels and virus titers were all upregulated when miR-146b-5p was overexpressed in DEFs. The opposite results were also observed upon knockdown of miR-146b-5p in DEFs. To explore the mechanism by which miR-146b-5p promoted DTMUV replication, mass spectrometry, and RNA pull-down assays were employed. Ribosomal protein S14 (RPS14), a component of 40S ribosomal proteins, was identified to interact with miR-146b-5p. In addition, the relative mRNA expression levels of RPS14 gene were negatively modulated by miR-146b-5p. Subsequently, it was found that overexpression of RPS14 could decrease the replication of DTMUV, and the reverse results were also detected by knockdown of RPS14. In conclusion, this study revealed that miR-146b-5p promoted DTMUV replication by targeting RPS14, which provides a new mechanism by which DTMUV evades host defenses and a new direction for further antiviral strategies development.
| S-EPMC10362356 | biostudies-literature
Project description:Ovarian cancer is a malignant gynecologic disease rarely diagnosed in the early stages. Among ovarian cancers, clear cell carcinoma has a poor prognosis due to its malignant potential. MicroRNAs (miRNAs) regulate gene expression in cells by suppressing the translation of the target gene or by degrading the target mRNA. They are also secreted from the cells in the blood, binding to the proteins or lipids and assisting in cell-cell communication. Hence, serum miRNAs can also be diagnostic biomarkers for ovarian cancer. This study investigated and identified specific miRNAs for ovarian clear cell carcinoma and compared them to those of ovarian endometrioma in healthy patients. CA125, an ovarian tumor marker, did not differ between patients with ovarian clear cell carcinoma, endometriosis, or healthy controls. Four miRNAs (miR-146a-5p, miR-191-5p, miR-484, and miR-574-3p) were analyzed. The miR-146a-5p and miR-191-5p expression levels were significantly increased in the serum samples from the patients with ovarian clear cell carcinoma compared to the healthy controls but not in the patients with endometriosis (P < 0.05). Furthermore, the bioinformatics analysis showed that CCND2 and NOTCH2 were the candidate target genes of miR 146a-5p and miR-191-5p. In conclusion, our results showed that miR 146a-5p and miR-191-5p might be useful as early and non-invasive diagnostic tools in ovarian clear cell carcinoma. These miRNAs can help in distinguishing between ovarian clear cell carcinoma and ovarian endometrioma. To the best of our knowledge, no studies have screened any candidates specifically for clear cell carcinoma.
2023-10-06 | GSE239685 | GEO