Dysregulation of principal circulating miRNAs in Nonhuman Primates following ischemic stroke
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA756250 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15526933.fastq.gz | Fastqsanger.gz | |||
| SRR15526934.fastq.gz | Fastqsanger.gz | |||
| SRR15526935.fastq.gz | Fastqsanger.gz | |||
| SRR15526936.fastq.gz | Fastqsanger.gz | |||
| SRR15526937.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Reactive astrocytes play critical roles after brain injury, but their precise function is not well defined, particularly in humans and nonhuman primates (NHPs). Here, we utilized single nuclei transcriptomics to characterize astrocytes after ischemic stroke in the primary visual cortex (V1) of the marmoset monkey. We observed nearly complete segregation between stroke and control astrocyte clusters. Screening the top 30 differentially expressed genes to identify candidates that might limit stroke recovery, we discovered that RTN4A/ NogoA, a neurite-outgrowth inhibitory protein previously associated specifically with oligodendrocytes but not astrocytes, was expressed in a majority of reactive astrocytes. Robust NogoA upregulation on reactive astrocytes following stroke was confirmed in both the marmoset and human brain, whereas rodents exhibited only a marginal change in NogoA expression following stroke. Further, in vivo and in vitro studies determined that NogoA mediated an anti-inflammatory response which likely contributes to limiting deeper infiltration of peripheral macrophages into the surviving parenchyma during the subacute post-stroke period. These findings are directly relevant to the development of NogoA-targeting therapies designed for clinical use shortly after ischemic stroke. In addition, our data have uncovered the complexity of astrocyte responses in primates, which highlights the importance of preclinical model selection for discovery research designed to identify novel therapeutics for brain injury.
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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.
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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 [RB1-inducible coiled-coil 1 (RB1CC1), G-protein subunit γ 5 (GNG5), and chemokine (C-X-C motif) receptor 4 (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.
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