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Genomewide expression profile of wire-injured carotid arteries harvested from either miR-126+/+/ApoE-/- or miR-126-/-/ApoE-/- mice during neointima development

ABSTRACT: We tried to identify mRNA targets of miR-126 involved in neointima formation in mice with an atherogenic background. Genome-wide expression profiling was carried out in wire-injured carotid arteries of miR-126+/+/ApoE-/- (control group) and miR-126-/-/ApoE-/- (target group) mice on western-type diet. RNA was isolated after 14 days following vascular injury (n=4 each group). Agilent SurePrint G3 Mouse GE Microarrays (8x60K format) were used in combination with a one-color based hybridization protocol. Signals on the microarrays were detected using the Agilent DNA Microarray Scanner. Differential gene expression was identified by applying appropriate biostatistics to the data set. GeneSpring GX11 analysis software was used to normalize and analyze the raw data

ORGANISM(S): Mus musculus

PROVIDER: GSE34262 | GEO | 2014/02/19

SECONDARY ACCESSION(S): PRJNA149967

REPOSITORIES: GEO

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Genomewide expression profile of wire-injured carotid arteries harvested from either miR-126+/+/ApoE-/- or miR-126-/-/ApoE-/- mice during neointima development

Project description:We tried to identify mRNA targets of miR-126 involved in neointima formation in mice with an atherogenic background. Genome-wide expression profiling was carried out in wire-injured carotid arteries of miR-126+/+/ApoE-/- (control group) and miR-126-/-/ApoE-/- (target group) mice on western-type diet. RNA was isolated after 14 days following vascular injury (n=4 each group). Agilent SurePrint G3 Mouse GE Microarrays (8x60K format) were used in combination with a one-color based hybridization protocol. Signals on the microarrays were detected using the Agilent DNA Microarray Scanner. Differential gene expression was identified by applying appropriate biostatistics to the data set. GeneSpring GX11 analysis software was used to normalize and analyze the raw data Genomewide expression profile of miR-126+/+/ApoE-/- and miR-126-/-/ApoE-/- mice were measured at 14 days after vascular injury . 4 animals per group were used.

2014-02-19 | E-GEOD-34262 | biostudies-arrayexpress

miRNA gene expression profile of ApoE-/- mice during neointima formation

Project description:In order to identify microRNAs involved in neointima formation in mice with an atherogenic background, wire-induced carotid injury was performed in ApoE-/- mice on western-type diet. Uninjured carotid arteries served as control. RNA was isolated after 1, 7, 14, and 28 days (n=3-4 each group) and hybridized to an Agilent microRNA microarray (Sanger v12). Significantly regulated microRNAs (>2-fold) over time (P<0.05; ANOVA and Benjamini-Hochberg correction) were clustered by K-means algorithm. Distinct groups of similarly regulated microRNAs were detected in the course of neointima formation in hyperlipidemic mice.

2014-11-28 | GSE34054 | GEO

Gene Expression Profile for the identification of miR-126 targets

Project description:"The analysis was designed to search for putative seed sequences for miR-126 in the 3’UTR of up-regulated genes. ECs were co-transfected with anti-miR-126 and a plasmid vector bearing the GFP-coding sequence and three complementary sites for miR-126 downstream. As a consequence of the presence of miR-126 binding sites the GFP expression was under the control of miR-126. Fluorescente cells were the cells transfected with anti-miR-126 oligo. MiR-126 target enrichment analysis was performed on the basis of the Miranda database, as provided by Diana miRGen. Significance was estimated on the basis of hyper geometric distribution p-values comparing the occurrence of miR targets in the signature with respect to the universe, defined as the genes expressed in HUVEC. Frequency of log 2 ratio between the subset of mir-126 targets and the genes which are not targets of miR-126 were plotted, highlighting enrichment of the target of miR in differentially regulated genes. "

2013-10-18 | GSE32089 | GEO

miR-126-126star in melanoma cell lines

Project description:Based on microRNA expression profiling studies, here we focus on miR-126&126* as the most downmodulated microRNAs in a panel of melanoma cell lines at different stages of progression compared with normal human melanocytes. At present no data exist on miR-126&126* possible role in melanoma. Our results show miR-126/miR-126* downregulation associated with tumor progression and the antineoplastic role deriving from their restored expression in metastatic melanomas in vitro as well as in vivo.

2013-05-21 | E-MEXP-3629 | biostudies-arrayexpress

miR-126 Governs Human Leukemia Stem Cell Quiescence and Therapeutic Resistance

Project description:In acute myeloid leukemia (AML), leukemia stem cells (LSC) play a central role in disease progression and recurrence due to their intrinsic capacity for self-renewal and chemotherapy resistance. Whereas epigenetic mechanisms balance normal blood stem cell self-renewal and fate decisions, mutation and dysregulation of epigenetic regulators are considered fundamental to leukemia initiation and progression. Alterations in miRNA function represent a non-canonical epigenetic mechanism influencing malignant hematopoiesis, however the function of miRNA in human LSC remains undetermined. Here we show that miRNA profiling of fractionated AML populations defines an LSC-specific signature that is highly prognostic for patient survival. Gain- and loss-of-function analyses demonstrated that miR-126 restrained cell cycle progression, prevented differentiation, and increased self-renewal of human LSC. By targeting the G0 to G1 gatekeeper CDK3, miR-126 preserved LSC quiescence and promoted chemotherapy resistance. Thus, in AML, miRNAs influence patient outcome through post-transcriptional regulation of stemness programs in LSC.

2016-03-31 | PXD001994 | Pride

Gene Expression Profile for the identification of miR-126 targets

Project description:"The analysis was designed to search for putative seed sequences for miR-126 in the 3M-bM-^@M-^YUTR of up-regulated genes. ECs were co-transfected with anti-miR-126 and a plasmid vector bearing the GFP-coding sequence and three complementary sites for miR-126 downstream. As a consequence of the presence of miR-126 binding sites the GFP expression was under the control of miR-126. Fluorescente cells were the cells transfected with anti-miR-126 oligo. MiR-126 target enrichment analysis was performed on the basis of the Miranda database, as provided by Diana miRGen. Significance was estimated on the basis of hyper geometric distribution p-values comparing the occurrence of miR targets in the signature with respect to the universe, defined as the genes expressed in HUVEC. Frequency of log 2 ratio between the subset of mir-126 targets and the genes which are not targets of miR-126 were plotted, highlighting enrichment of the target of miR in differentially regulated genes. " 3 x biological replicates of transiently trasfected cells with anti miR-126 oligo (LNA), and controls oligo. 2 biological replicates for GFP are included as technical controls.

2013-10-18 | E-GEOD-32089 | biostudies-arrayexpress

Both gain and loss of function of miR-126 promote t(8;21) leukemia progression with different consequences and through different mechanisms

Project description:To investigate the pathological effect of miR-126 on the progression of acute myeloid leukemia (AML) induced by AML1-ETO9a (AE9a), we conducted a series of mouse bone marrow transplantation (BMT) assays with the following groups: AE9a (primary donor cells were wild-type mouse bone marrow progenitor (i.e., lineage negative; Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), AE9a+miR-126 (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a-miR-126), and miR-126KO+AE9a (primary donor cells were miR-126 knockout mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), along with a control group (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG empty vector). The control group was only used in the primary and secondary BMT assays, whereas the three leukemic groups including AE9a, AE9a+miR-126 and miR-126KO+AE9a were used in four passages (i.e., primary, secondary, tertiary and quaternary) of BMT assays. Then, gene expression profiling was conducted with bone marrow samples collected from different groups to decipher the molecular mechanisms underlying miR-126 effects on leukemia initiation and progression and maintenance and self-renewal of leukemia stem/initiating cells.

2015-09-07 | GSE65939 | GEO

Regulation of zebrafish endothelial gene expression by miR-126

Project description:Fish, JE, Santoro, MM, Morton, SU, Yu, S, Yeh, RF, Wythe, JD, Ivey, KI, Bruneau, BG, Stainier, DYR, and Srivastava, D. (2008). miR-126 Regulates Angiogenic Signaling and Vascular Integrity. Developmental Cell 15, 272-284. Precise regulation of the formation, maintenance, and remodeling of the vasculature is required for normal development, tissue response to injury, and tumor progression. How specific microRNAs intersect with and modulate angiogenic signaling cascades is unknown. Here, we identified microRNAs that were enriched in endothelial cells derived from mouse embryonic stem (ES) cells and in developing mouse embryos. We found that miR-126 regulated the response of endothelial cells to VEGF. Additionally, knockdown of miR-126 in zebrafish resulted in loss of vascular integrity and hemorrhage during embryonic development. miR-126 functioned in part by directly repressing negative regulators of the VEGF pathway, including the Sprouty-related protein SPRED1 and phosphoinositol-3 kinase regulatory subunit 2 (PIK3R2/p85-β). Increased expression of Spred1 or inhibition of VEGF signaling in zebrafish resulted in defects similar to miR-126 knockdown. These findings illustrate that a single miRNA can regulate vascular integrity and angiogenesis, providing a new target for modulating vascular formation and function.

2008-08-12 | GSE12012 | GEO

Regulation of human endothelial gene expression by miR-126

2008-08-12 | GSE12011 | GEO

miR-126 over-expression in highly metastatic LM2 breast cancer cells.

Project description:miR-126 were over-expressed using the miR-Vec system in highly metastatic LM2 cells. The LM2 cell line are described in detail in Minn et al. Nature 2005 This approach was used to conduct an unbiased search for specific miR-126 target genes in breast cancer cells.

2011-12-16 | GSE23905 | GEO

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