Specific stroke-induced miRNAs could mediate and interaction between peripheral blood and the brain
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ABSTRACT:
PROVIDER: PRJNA965813 | ENA |
REPOSITORIES: ENA
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Project description:Ischemic stroke is a major public health problem that is currently among the top leading causes of serious, long-term disability worldwide. The lack of effective treatment strategies prompted a search for new molecular targets for stroke prognosis and therapy. One of the epigenetic mechanisms controlling stroke progression and recovery involves signaling pathways mediated by short non-coding RNAs called microRNAs (miRNAs). Recent studies demonstrated stroke-specific changes in miRNA expression. The main goal of the present study was identify miRNAs mediating a communication between the brain and peripheral circulation in human stroke.
2023-05-31 | GSE231431 | GEO
Project description:To understand the differentially expressed miRNAs in the peripheral blood CD34+ cells after stroke (first 24 hours after symptom onset), we have employed mRNA sequencing. Among 45 patients included in the study, 6 patients were chosen depending on the clinical outcome (3 patients with "good" and 3 patients with "bad" clinical outcome after 3 months). Immediately after the collection of the peripheral blood from the patients, mononuclear cells (MNCs) were isolated by density centrifugation. Then, CD34+ cells were isolated from MNCs using MACS columns. The cells were immediately frozen in RNAProtect Cell Reagent. The cell samples were shipped to Seqmatic LLC (Fremont, CA, USA) for RNA isolation and miRNA sequencing. RNA integrity measurements, library preparation and next generation sequencing were conducted at Seqmatic LLC, CA, USA.
2018-08-02 | GSE85299 | GEO
Project description:The purpose of this project was to elucidate gene expression in the peripheral whole blood of acute ischemic stroke patients to identify a panel of genes for the diagnosis of acute ischemic stroke. Peripheral blood samples were collected in Paxgene Blood RNA tubes from stroke patients who were >18 years of age with MRI diagnosed ischemic stroke and controls who were non-stroke neurologically healthy. The results suggest a panel of genes can be used to diagnose ischemic stroke, and provide information about the biological pathways involved in the response to acute ischemic stroke in humans. Total RNA extracted from whole blood in n=39 ischemic stroke patients compared to n=24 healthy control subjects.
2010-06-08 | E-GEOD-16561 | biostudies-arrayexpress
Project description:The purpose of this project was to elucidate gene expression in the peripheral whole blood of acute ischemic stroke patients to identify a panel of genes for the diagnosis of acute ischemic stroke. Peripheral blood samples were collected in Paxgene Blood RNA tubes from stroke patients who were >18 years of age with MRI diagnosed ischemic stroke and controls who were non-stroke neurologically healthy. The results suggest a panel of genes can be used to diagnose ischemic stroke, and provide information about the biological pathways involved in the response to acute ischemic stroke in humans.
2010-06-01 | GSE16561 | GEO
Project description:Despite the recent interest in plasma microRNA (miRNA) biomarkers in acute ischemic stroke patients, there is limited knowledge about the miRNAs directly related to stroke itself due to the multiple complications in patients, which has hindered the research progress of biomarkers and therapeutic targets of ischemic stroke. Therefore, in this study, we compared the differentially expressed miRNA profiles in the plasma of three rhesus monkeys pre- and post-cerebral ischemia. After cerebral ischemia, RFAM sequence category revealed increased ribosomic RNA (rRNA) and decreased transfer RNAs (tRNAs) in plasma. Of the 2049 miRNAs detected after cerebral ischemia, 36 were upregulated, and 76 were downregulated (fold change ≥2.0, P <0.05). For example, Mml-miR-191-5p, miR-421, miR-409-5p, and let-7g-5p were found to be significantly overexpressed, whereas mml-miR-128a-5p_R-2, miR-431_R-1, and let-7g-3p_1ss22CT were significantly downregulated. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed that these differentially expressed miRNAs were implicated in the regulation of ubiquitin-mediated proteolysis and signaling pathways in cancer, glioma, chronic myeloid leukemia, and chemokine signaling. miRNA clustering analysis showed that mml-let-7g-5p and let-7g-3p_1ss22CT, which share three target genes (RB1CC1, GNG5, and CXCR4), belong to one cluster, were altered in opposite directions following ischemia. These data suggest that circulating mml-let-7g may serve as a therapeutic target for ischemic stroke.
2021-08-27 | GSE182429 | GEO
Project description:Purpose: Signaling pathways mediated by microRNAs (miRNAs) represent one of the mechanisms that regulate stroke progression and recovery. The goal of this study is to investigate miRNA expression signatures in freshly removed human stroke brain tissue. Methods: Human brain samples (5 stroke and 3 non-stroke samples) obtained at 48-72 hours after stroke onset during craniectomy and stroke-ectomy, were subjected to histopathological and immunofluorescence microscopy analyses. NGS sequencing was performed by Qiagen company and analyses were carried out using QIAseq miRNA Quantification workflow and RNA-seq Analysis tools within CLC Genomics Workbench (version 20.0.2). Reads were normalized for expression analysis using trimmed mean of M-values method (TMM). miRNA profiling was performed using the EdgeR in Bioconductor package. Whole transcriptome RNA-sequencing Analysis: The unmapped reads from the NGS miRNA analysis were extracted, deduplicated and mapped to the genome. Gene expressions were calculated by counting number of reads mapping to the annotated gene loci. Human miR-155 Targets RT2 Profiler PCR Array (Qiagen) was performed using 3 RNA samples per stroke and control groups. The PCR Array Data analysis was performed using an automated PCR Analysis Web Portal and GeneGlobe Data Analysis (Qiagen). Results: Human stroke brain tissue was characterized by classic ischemic changes, including significant neuronal and vascular damage, and prominent edema. The absence of monocytes and notable neutrophil infiltration indicated the early stage of leukocyte response to ischemia. miRNA NGS analysis detected 36 miRNAs with significantly aberrant expression in stroke tissue, as compared to non-stroke samples. Of these miRNAs, 19 were previously identified in stroke patient blood and CSF, while dysregulation of 16 miRNAs was newly detected in this study. Bioinformatics pathway enrichment analysis demonstrated a strong association of the identified miRNAs with stroke-related biological processes and signaling pathways Conclusions: Dysregulated miRNAs detected in our study could be regarded as potential candidates for biomarkers and/or targets for therapeutic intervention. The obtained data will serve for better understanding of the molecular basis of stroke and provide valuable information for the future functional studies in the experimental models of stroke.
2020-07-29 | GSE155257 | GEO
Project description:Few have characterized miRNA expression during the transition from injury to neural repair and secondary neurodegeneration following stroke in humans. We compared expression of 754 miRNAs from plasma samples collected 5, 15, and 30 days post-ischemic stroke from a discovery cohort (n=55) and 15-days post-ischemic stroke from a validation cohort (n=48) to healthy control samples (n=55 and 48 respectively) matched for age, sex, race and cardiovascular comorbidities using qRT-PCR. Eight miRNAs remained significantly altered across all time points in both cohorts including many described in acute stroke. The number of significantly dysregulated miRNAs more than doubled from post-stroke day 5 (19 miRNAs) to days 15 (50 miRNAs) and 30 (57 miRNAs). Twelve brain-enriched miRNAs were significantly altered at one or more time points (decreased expression, stroke versus controls: miR-107; increased expression: miR-99-5p, miR-127-3p, miR-128-3p, miR-181a-3p, miR-181a-5p, miR-382-5p, miR-433-3p, miR-491-5p, miR-495-3p, miR-874-3p, and miR-941). Many brain-enriched miRNAs were associated with apoptosis over the first month post-stroke whereas other miRNAs suggested a transition to synapse regulation and neuronal protection by day 30. These findings suggest that a program of decreased cellular proliferation may last at least 30 days post-stroke, and points to specific miRNAs that could contribute to neural repair in humans.
2023-10-04 | GSE244632 | GEO
Project description:Previous research has suggested the potential of esketamine in alleviating post-stroke neuroinflammation, yet the underlying mechanism remained elusive. In our research, we have observed that esketamine increased the number of M2 anti-inflammatory phenotype microglia in the infarcted area after stroke, and this phenomenon is partly associated with the suppression of Panx1. Further research revealed that esketamine suppresses the phosphorylation of sarcoma kinase (Src) at the tyrosine 416 (Y416) site and inhibits the interaction between Src and Panx1, ultimately suppressing the function of Panx1. However, we found esketamine's inhibitory effect on post-stroke Panx1 activation is the underlying mechanism driving the increase in unactivated microglia, yet esketamine's influence on microglial polarization is mediated through a mechanism independent of Panx1.Our research suggests that esketamine, as a drug already used in clinical anesthesia, could potentially provide a solution during the periprocedural period to mitigate the damage caused by aseptic inflammation post-stroke.
2024-09-17 | GSE277009 | GEO
Project description:Analysis of microglial gene expression profiles after ischemic stroke. Stroke is a complicated disease caused by the interaction of multiple celltypes. Results provide new insights into the molecular mechanisms underlying microglial activation after ischemic stroke.
2022-01-01 | GSE172456 | GEO
Project description:Analysis of astrocytic gene expression profiles after ischemic stroke. Stroke is a complicated disease caused by the interaction of multiple celltypes. Results provide new insights into the molecular mechanisms underlying astrocytic activation after ischemic stroke.
2024-05-23 | GSE238125 | GEO