Analysis of differentially expressed genes in KYSE450 cell line after tranfection with miR-107, miR-198 and miR-214.
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE93756 | GEO | 2019/01/17
REPOSITORIES: GEO
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Project description:Analysis of differentially expressed genes in KYSE450 cell line after tranfection with miR-107, miR-198 and miR-214.
| PRJNA362301 | ENA
Project description:Despite increasing understanding of the prognostic importance of vascular stiffening linked to perivascular fibrosis in hypertension, the molecular and cellular regulation of this process is poorly understood. We aimed to study the functional role of microRNA-214 (miR-214) in the induction of perivascular fibrosis and endothelial dysfunction driving vascular stiffening. Out of 381 miRs screened in the perivascular tissues (PVAT) in response to angiotensin II (Ang II)-mediated hypertension, miR-214 showed the highest induction (8-fold, p<0.01). MiR-214 induction was pronounced in perivascular and circulating T cells, but not in PVAT adipocytes. Global deletion of miR-214-/- prevented Ang II-induced periaortic fibrosis Col1a1, Col3a1, Col5a1 and Tgfb1 expression, hydroxyproline accumulation and vascular stiffening, without difference in blood pressure. Mechanistic studies revealed that miR-214-/- mice were protected against endothelial dysfunction, oxidative stress and increased Nox2, all of which were induced by Ang II in WT mice. Ang II-induced recruitment of T cells into PVAT was abolished in miR-214-/- mice. Adoptive transfer of miR-214-/- T cells into RAG1-/- mice resulted in reduced perivascular fibrosis compared to the effect of WT T cells. Ang II induced hypertension caused significant change in the expression of 1380 T cell genes in WT, but only 51 in miR-214-/-. T cell activation, proliferation and chemotaxis pathways were differentially affected. miR-214-/- prevented Ang II-induction of pro-fibrotic T cell cytokines (IL-17, TNF, IL-9 and IFN) and chemokine receptors (CCR1, CCR2, CCR4, CCR5, CCR6 and CXCR3). This manifested in reduced in vitro and in vivo T cell chemotaxis resulting in attenuation of profibrotic perivascular inflammation. Translationally, we show that miR-214 is increased in plasma of hypertensive patients and is directly correlated to pulse wave velocity as a measure of vascular stiffness.
2020-02-29 | GSE143809 | GEO
Project description:Animals were sc dosed with 5mg/kg anti-miR-214 or control anti-miR, had UUO performed and were sacrificed at 7 days.
2013-11-05 | GSE48194 | GEO
Project description:We aimed to detect the mRNA expression levels in HepG2 cells after trasfection with NC RNA, miR-214 mimics or PVT1 siRNAs.
2020-12-12 | GSE123745 | GEO
Project description:We treated horse mammary derived epithelial cells (MDECs) with either a miR-214-3p mimic or a negative mimic control in the presence of the carcinogenic agent DMBA. Over expression of miR-214-3p suppressed cell apoptosis compared to the control, and suggests a potential oncogenic role in breast cancer.
2023-10-11 | GSE189879 | GEO
Project description:Animals were sc dosed with 5mg/kg anti-miR-214 or control anti-miR, had UUO performed and were sacrificed at 7 days. n=4 animals per group, 2 groups
2013-11-05 | E-GEOD-48194 | biostudies-arrayexpress
Project description:Using anti-Argonaute (anti-AGO) antibody co-immunoprecipitation, followed by microarray analyses and downstream bioinformatics, ‘RIP-Chip’ experiments enable direct analyses of miRNA targets. The analyses support four major findings: (i) RIP-Chip studies correlated with total input mRNA profiling provides more comprehensive information than using either RIP-Chip or total mRNA profiling alone after miRNA transfections; (ii) new data confirm that miR-107 paralogs target coding sequence (CDS) of mRNA; (iii) biochemical and computational studies indicate that the 3′ portion of miRNAs plays a role in guiding miR-103/7 to the CDS of targets; and (iv) there are major sequence-specific targeting differences between miRNAs in terms of CDS versus 3′-untranslated region targeting, and stable AGO association versus mRNA knockdown. For detailed protocol and for full discussion of the results please see Nelson PT et al, Nucleic Acids Res. 2011 Oct;39(18):8163-72. Affymetrix microarrays which were performed 2 days following miRNA transfections: total lysate following miRNA-like transfections; and RNA from anti-Argonaute (2A8 monoclonal antibody) co-Ips RIP-ChIP studies (and parallel assessments of total input mRNA) were performed in cultured H4 cells after transfection with miRNAs corresponding to the miR-15/107 gene group (miR-103, miR-107, miR-16 and miR-195), another physiological miRNA (miR-320), miR-15b*, and three non-physiological additional miRNA-like molecules (miR-107-mut1, mir-107-mut2, and negative control miRNA from Ambion). For details on transfected miRNA sequences, see Nelson PT et al, Nucleic Acids Res. 2011 Oct;39(18):8163-72. Three biological replicates were run for each condition with a total of 54 separate human Affymetrix Human Gene 1.0 ST array replicates. See Wang WX et al, RNA (2010) 16:394-404 for detailed protocol of RIP-ChIP.
2012-12-11 | E-GEOD-42823 | biostudies-arrayexpress
Project description:The viral miRNA miR-K6-5p encoded by the DNA tumor virus Kaposi’s sarcoma-associated herpesvirus exhibits offset, sequence similarity with the tumor suppressive cellular miR-15/16 family, as well as sharing a short seed match to the cellular miR-214 (nts 2-7). We investigated how gene regulation by the viral miR-K6-5p is related to regulation by these cellular miRNAs by performing transcriptome analysis. mRNA-Seq was done in HEK 293T NoDice cells (Bogerd et al., RNA 2014) lacking Dicer which severely impaired the maturation of miRNAs thereby eliminating confounding effects of endogenously expressed miR-15/16 family. We transfected mature miRNA mimics of miR-16, miR-K6-5p wild-type, a variant of miR-K6-5p with a U at nt 1 instead of a C to control of RISC loading (miR-K6 5’U), miR-214, or a control mimic into NoDice cells, and harvested total RNA 2 days post-transfection.
2019-11-01 | GSE128576 | GEO
Project description:Early reperfusion of ischemic cardiac tissue remains the most effective intervention for improving clinical outcome following myocardial infarction. However, abrupt increases in intracellular Ca2+ during myocardial reperfusion cause cardiomyocyte death and consequent loss of cardiac function, referred to as ischemia/reperfusion (IR) injury. Cardiac IR is accompanied by dynamic changes in expression of microRNAs (miRNAs), which inhibit specific mRNA targets. miR-214 is up-regulated during ischemic injury and heart failure in mice and humans, but its potential role in these processes is unknown. We show that genetic deletion of miR-214 in mice causes loss of cardiac contractility, increased apoptosis, and excessive fibrosis in response to IR injury. The microarray contains 6 samples, each containing cDNA pooled from 3 mice per group. There are no replicates. The array was designed to make 3 different pairwise comparisons between the following: P14 WT and miR-214 KO hearts; adult WT and miR-214 KO skeletal muscle; adult WT and miR-214 KO hearts
2012-01-31 | E-GEOD-35421 | biostudies-arrayexpress
Project description:To identify putative novel specific targets of miR-199-5p, miR-199a-3p and miR-214-3p, we overexpressed these miRNAs in human MRC5 pulmonary fibroblasts (CCL-171) using synthetic pre-miRNAs or a synthetic “negative” pre-miRNA control (miR-Neg). RNA samples were harvested 48 hours post-transfection and 3 independent experiments were carried out.
2019-04-11 | GSE97824 | GEO