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2,648
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Dataset results
2,648 results for “MIR”
Adjuvant IFN-α for Patients Underwent Curative Surgery for HCC With a Low miR-26 Expression
ClinicalTrials.gov study NCT01681446. IPD Sharing: Not stated. Countries: 1. Publications: 7.
MIRs 04 : Interpectoral Nerve Block With Ropivacaine Versus Placebo Before Breast Cancer Surgery
ClinicalTrials.gov study NCT04327063. IPD Sharing: YES. Countries: 1. Publications: 1.
Evaluation of ProALL miRs in Blood Specimen for Prediction of ALL Relapse Risk
ClinicalTrials.gov study NCT03000335. IPD Sharing: NO. Countries: 1. Publications: 8.
miR-200b & miR-21 in Diabetic Wounds
ClinicalTrials.gov study NCT02581098. IPD Sharing: Not stated. Countries: 1. Publications: 14.
Evaluation of Safety & Efficacy of MIR 19 ® Inhalation Solution in Patients With Moderate COVID-19
ClinicalTrials.gov study NCT05184127. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Clinical Significance of Hepatic and Circulating microRNAs miR-221 and miR-222 in Hepatocellular Carcinoma
ClinicalTrials.gov study NCT02928627. IPD Sharing: NO. Countries: 1. Publications: 3.
The Mechanism of lncRNA NEAT1 in Alleviating Acute Respiratory Distress Syndrome Through miR-27b Regulated Nrf2 Pathway
ClinicalTrials.gov study NCT04937855. IPD Sharing: Not stated. Countries: 1. Publications: 19.
Data from: Despite high levels of expression in thymic epithelial cells, miR-181a1 and miR-181b1 are not required for thymic development
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Data from: GATA2 controls lymphatic endothelial cell junctional integrity and lymphovenous valve morphogenesis through miR-126
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miR-1285-3p targets TPI1 to regulate the glycolysis metabolism signaling pathway of Tibetan sheep Sertoli cells
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Circulating myeloid-derived suppressor cells facilitate invasion of thyroid cancer cells by repressing miR-486-3p
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Data from: A short peptide exerts neuroprotective effects on cerebral ischemia-reperfusion injury by reducing inflammation via the miR-6328/IKKβ/NF-κB axis
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Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease
Canine myxomatous mitral valve disease (MMVD) resembles the early stages of myxomatous pathology seen in human non-syndromic mitral valve prolapse, a common valvular heart disease in the adult human population. Canine MMVD is seen in older subjects, suggesting age-related epigenetic dysregulation leading to derangements in valvular cell populations and matrix synthesis or degradation. We hypothesized that valvular interstitial cells (VICs) undergo disease-relevant changes in miRNA expression. In primary VIC lines from diseased and control valves, miRNA expression was profiled using RT-qPCR and next generation sequencing. VICs from diseased valves showed phenotypic changes consistent with myofibroblastic differentiation (vimentinlow+, a-SMAhigh+), increases in senescence markers (p21, SA-b-gal), and decreased cell viability and proliferation potential. RT-qPCR and miRNA sequencing analyses both showed significant (p<0.05) downregulation of let-7c, miR-17, miR-20a, and miR-30d in VICs from diseased valves compared to controls. Decreased let-7c, miR-17, and miR-20a may contribute to myofibroblastic differentiation in addition to cell senescence, and decreased miR-30d may disinhibit cell apoptosis. These data support the hypothesis that epigenetic dysregulation plays an important role in age-related canine MMVD.
Data from: Inhibition of Smurf2 translation by miR-322/503 protects from ischemia reperfusion injury by modulating EZH2/Akt/GSK3β signaling
BACKGROUND: myocardial ischemia/reperfusion (I/R) is a common and lethal disease that threatens people's life worldwide. The underlying mechanisms are under intensive study and yet remain unclear. Here, we explored the function of miR-322/503 in myocardial I/R injury. METHODS: We used isolated rat perfused heart as an in vivo model and H9c2 cells subjected with the oxygen and glucose deprivation followed by reperfusion (OGD/R) as in vitro model to study myocardial I/R injury. TTC staining was used to measure the infarct size and TUNEL staining was used to examine apoptosis. qRT-PCR and western blot were used to determine expression levels of miR-322/503, Smurf2, EZH2, p-Akt, p-GSK3β. RESULTS: Overexpression of miR-322/503 decreased infarct size, inhibited cell apoptosis and promoted cell proliferation through up-regulation of p-Akt and p-GSK3β. Thus, the expression of miR-322/503 was reduced during I/R process. On the molecular level, miR-322/503 directly bound Smurf2 mRNA and suppressed its translation. Smurf2 ubiquitinated EZH2 and degraded EZH2 which could activate Akt/GSK3β signaling. CONCLUSIONS: Our study demonstrates that miR-322/503 plays a beneficial role in myocardial I/R injury. By inhibition of Smurf2 translation, miR-322/503 induces EZH2 expression and activates Akt/GSK3β pathway, thereby protecting cells from ischemia reperfusion injury.
Data from: Arsenic induces members of the mmu-miR-466-669 cluster which reduces NeuroD1 expression
Chronic arsenic exposure can result in adverse development effects including decreased intellectual function, reduced birth weight, and altered locomotor activity. Previous in vitro studies have shown that arsenic inhibits stem cell differentiation. MicroRNAs (miRNAs) are small non-coding RNAs that regulate multiple cellular processes including embryonic development and cell differentiation. The purpose of this study was to examine whether altered miRNA expression was a mechanism by which arsenic inhibited cellular differentiation. The pluripotent P19 mouse embryonal carcinoma cells were exposed to 0 or 0.5 μM sodium arsenite for 9 days during cell differentiation, and changes in miRNA expression was analyzed using microarrays. We found that the expression of several miRNAs important in cellular differentiation, such as miR-9 and miR-199 were decreased by 1.9- and 1.6-fold respectively following arsenic exposure, while miR-92a, miR-291a, and miR-709 were increased by 3-, 3.7- and 1.6-fold, respectively. The members of the miR-466-669 cluster and its host gene, Scm-Like with four Mbt domains 2 (Sfmbt2), were significantly induced by arsenic from 1.5- to 4-fold in a time-dependent manner. Multiple miRNA target prediction programs revealed that several neurogenic transcription factors appear to be targets of the cluster. When consensus anti-miRNAs targeting the miR-466-669 cluster were transfected into P19 cells, arsenic-exposed cells were able to more effectively differentiate. The consensus anti-miRNAs appeared to rescue the inhibitory effects of arsenic on cell differentiation due to an increased expression of NeuroD1. Taken together, we conclude that arsenic induces the miR-466-669 cluster, and that this induction acts to inhibit cellular differentiation in part due to a repression of NeuroD1.
Data from: miR-122, small RNA annealing and sequence mutations alter the predicted structure of the Hepatitis C virus 5′ UTR RNA to stabilize and promote viral RNA accumulation
Annealing of the liver-specific microRNA, miR-122, to the Hepatitis C virus (HCV) 5′ UTR is required for efficient virus replication. By using siRNAs to pressure escape mutations, 30 replication-competent HCV genomes having nucleotide changes in the conserved 5′ untranslated region (UTR) were identified. In silico analysis predicted that miR-122 annealing induces canonical HCV genomic 5′ UTR RNA folding, and mutant 5′ UTR sequences that promoted miR-122-independent HCV replication favored the formation of the canonical RNA structure, even in the absence of miR-122. Additionally, some mutant viruses adapted to use the siRNA as a miR-122-mimic. We further demonstrate that small RNAs that anneal with perfect complementarity to the 5′ UTR stabilize and promote HCV genome accumulation. Thus, HCV genome stabilization and life-cycle promotion does not require the specific annealing pattern demonstrated for miR-122 nor 5′ end annealing or 3′ overhanging nucleotides. Replication promotion by perfect-match siRNAs was observed in Ago2 knockout cells revealing that other Ago isoforms can support HCV replication. At last, we present a model for miR-122 promotion of the HCV life cycle in which miRNA annealing to the 5′ UTR, in conjunction with any Ago isoform, modifies the 5′ UTR structure to stabilize the viral genome and promote HCV RNA accumulation.
Raw data for the article: MicroRNA-30d and -483-3p for bi-ventricular remodelling and miR-126-3p for pulmonary hypertension in advanced heart failure
<p><strong>Aims: </strong>MicroRNAs play a role in pathogenic mechanisms leading to heart failure. We measured a panel of 754 miRNAs in the myocardial tissue and in the serum of patients with heart failure with reduced ejection fraction due to dilatative idiopathic cardiomyopathy (DCM, N = 10) or ischaemic cardiomyopathy (N = 3), referred to left ventricular assist device implant. We aim to identify circulating miRNAs with high tissue co-expression, significantly associated to echocardiographic and haemodynamic measures.</p> <p><strong>Methods and results: </strong>We have measured a panel of 754 miRNAs in the myocardial tissue [left ventricular (LV) apex] and in the serum obtained at the same time in a well selected study population of end-stage heart failure with reduced ejection fraction due to either DCM or ischaemic cardiomyopathy, referred to continuous flow left ventricular assist device implant. We observed moderate agreement for miR-30d, miR-126-3p, and miR-483-3p. MiR-30d was correlated to LV systolic as well as diastolic volumes (r = 0.78, P = 0.001 and r = 0.80, P = 0.005, respectively), while miR-126-3p was associated to mPAP and PCWP (r = -0.79, P = 0.007 and r = -0.80, P = 0.005, respectively). Finally, serum miR-483-3p had an association with right ventricular end diastolic diameter (r = -0.73, P = 0.02) and central venous pressure (CVP) (r - 0.68 p 0.03).</p> <p><strong>Conclusions: </strong>In patients with DCM, few miRNAs are co-expressed in serum and tissue: They are related to LV remodelling (miR-30d), post-capillary pulmonary artery pressure (miR-126-3p), and right ventricular remodelling/filling pressures (miR-483-3p). Further studies are needed to confirm their role in diagnosis, prognosis or as therapeutic targets in heart failure with reduced ejection fraction.</p>
raw data - circNR3C2 promote chondrogenic differentiation and cartilage repair of human adipose-derived stem cells via hsa-miR-647/SOX9 pathway
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Data from: Downregulation of circATXN7 represses non-small cell lung cancer growth by releasing miR-7-5p
<p>Circular RNAs (circRNAs) participate in the occurrence and progression of many cancers. CircRNA ataxin 7 (circATXN7) (circBase ID: hsa_circ_0066436) plays a promoting influence on gastric cancer progression. However, the biological role of circATXN7 in non-small cell lung cancer (NSCLC) is indistinct. CircATXN7 and PFN2 were highly expressed in NSCLC, whereas miR-7-5p expression had the opposite trend. CircATXN7 overexpression constrained apoptosis and promoted proliferation, metastasis, invasion, and epithelial-mesenchymal transition (EMT) of NSCLC cells, but circATXN7 silencing played the opposing influence and repressed xenograft tumor growth <i>in vivo</i>. CircATXN7 served as a miR-7-5p sponge, and circATXN7 regulated malignant behaviors of NSCLC cells through sponging miR-7-5p. PFN2 acted as a miR-7-5p target. PFN2 silencing overturned the promoting effect of miR-7-5p inhibitor on NSCLC cell malignancy, while PFN2 overexpression reversed the inhibitory impact of miR-7-5p mimic on NSCLC cell malignancy. CircATXN7 accelerated the malignancy of NSCLC cells through adsorbing miR-7-5p and upregulating PFN2, offering evidence to support circATXN7 as a might target for NSCLC treatment.</p>
Pan-Cancer analysis of miR-15/miR-107 family uncovers miR-497-5p and miR-195-5p as biomarkers in multiple cancers
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.