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Profiling study of B cells from lymph nodes in miR-146a over-expression transgenic mice

ABSTRACT: B cells were isolated from wild type and miR-146a transgenic mice, and analyzed using microarray assay.WT1 and WT2 were samples repeats, so were TG1 and TG2 .

ORGANISM(S): Mus musculus

PROVIDER: GSE39779 | GEO | 2012/08/08

SECONDARY ACCESSION(S): PRJNA172114

REPOSITORIES: GEO

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Profiling study of B cells from lymph nodes in miR-146a over-expression transgenic mice

Project description:B cells were isolated from wild type and miR-146a transgenic mice, and analyzed using microarray assay.WT1 and WT2 were samples repeats, so were TG1 and TG2 . Each probe ID of a mouse transcript was ranked by fold change from up to down-regulated comparing to WT control. Sylamer miRNA seed enrichment analysis was performed with Markov correction as described (Nature Method 2008). WT vs. TG.

2012-08-07 | E-GEOD-39779 | biostudies-arrayexpress

Follicular B (FoB) cells purified from miR-17-92 transgenic mice, stimulated with LPS/IL-4 for 13.5 or 25.5 hours

Project description:We have generated a miR-17-92 transgenic allele (termed miR-17-92 Tg) whose expression can be turned on conditionally by Cre recombinase (Xiao et al, Nature Immunology, 9:405-14, 2008). The mice were crossed to CD19-Cre mice to turn on the transgene expression specifically in B cells. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 Tg/Tg mice (TG1, TG2, TG3) and miR-17~92 Tg/Tg mice (WT1, WT2, WT3) by MACS depletion of cells positive for CD5, CD43, and CD93 (also known as AA4.1). The purified B cells were stimulated with LPS/IL-4 for 13.5hr or 25.5hr. The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

2014-04-01 | E-GEOD-56377 | biostudies-arrayexpress

Transcription profiling by array of human Jurkat T cells either over-expressing miR-146a or with miR-146a knockdown

Project description:Screening the differetial expressed genes with Jurkat-146a(miR-146a over expression),Jurkat-sponge(miR-146a knockdown),Jurkat-FF3(vector control)

2010-03-24 | E-MEXP-2627 | biostudies-arrayexpress

Expression data of wildtype and miR-146a-deficient 2D2 transgenic T cells

Project description:We used the Affymetrix GeneChip Mouse Genome 430 2.0 Arrays to compare the gene expression profiles of wildtype and miR-146a-deficient 2D2 transgenic T cells.

2017-09-05 | GSE101165 | GEO

miR-146a regulates many lncRNAs in RAS induced senescence [Anti-146a]

Project description:miR-146a is a known anti-inflammatory miRNA. Intringuigly, it is overexpressed in RAS-induced senescent cells which is accompanied with a rich pro-inflammatoy secretpry phenotype. We aim to study possible sponges for miR-146a.

2021-05-11 | GSE150325 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Thymic Transcriptomes from Wild Type and Mir-146a Transgenic Mice

Project description:Purpose: To find out the global transcriptomic change induced by overexpression of miR-146a in thymus Methods:Thymic mRNA profile of two pools from age (five to six-week old)- and gender (one male and one female for each pool)- matched wild-type (WT) and miR-146a transgenic (Tg) mice were generated by deep sequencing using Illumina HiSeq 2500. The clean reads that passed quality filters were mapped against Mus musculus genome using HotHap2, and the only uniquely mapped reads were used to calculate reads per kilobase of exon per million fragment (RPKM) values for each sample. The transcript isoform with a fold-change over 2 and q<0.001 were considered differentially expressed. Conclusion: Our study identified 101 differently expressed transcripts in thymus from miR-146a Tg mice, including 56 down-regulated transcripts covering 49 genes which are the candidate targets of miR-146a

2018-02-14 | GSE99428 | GEO

Over-expression of miR-146a in basal-like breast cancer cells confers enhanced tumorigenic potential in association with altered p53 status

Project description:The tumor suppressor p53 is the most frequently mutated gene in human cancers, mutated in 25-30% of breast cancers. However, mutation rates differ according to breast cancer subtype, being more prevalent in aggressive estrogen receptor (ER) negative tumors, basal-like and HER2 amplified subtypes. This heterogeneity suggests that p53 may function differently across breast cancer subtypes. We used RNAi-mediated p53 knockdown (KD) and antagomir-mediated KD of microRNAs to study how gene expression and cellular response to p53 loss differ in luminal vs. basal-like breast cancer. As expected, p53 loss caused down regulation of established p53 targets (e.g. p21 and miR-34 family) and increased proliferation in both luminal and basal-like cell lines. However, some p53-dependent changes were subtype-specific, including expression of miR-134, miR-146a, and miR-181b. To study the cellular response to miR-146a upregulation in p53-impaired basal-like lines, antagomir knockdown of miR-146a was performed. KD of miR-146a caused decreased proliferation and increased apoptosis, effectively ablating the effects of p53 loss. Furthermore, we found that miR-146a upregulation decreased NF-kB expression and downregulated the NF-kB-dependent extrinsic apoptotic pathway (including TNF, FADD, and TRADD) and antagomir-mediated miR-146a KD restored expression of these components, suggesting a plausible mechanism for miR-146a-dependent cellular responses. These findings are relevant to human basal-like tumor progression in vivo, since miR-146a is highly expressed in p53-mutant basal-like breast cancers. These findings suggest that targeting miR-146a expression may have value for altering the aggressiveness of p53 mutant basal-like tumors.

2014-06-30 | GSE52783 | GEO

Data in support of Absence of miRNA-146a differentially alters microglia function and proteome

Project description:MiR-146a is an important regulator of innate inflammatory responses and is also implicated in cell death and survival. Here, we identified microglia as the main cellular source of miR-146a among mouse CNS resident cells. We further characterized the phenotype of miR-146a KO microglia cells during in vivo demyelination induced by cuprizone (CPZ) and found reduced number of CD11c+ microglia in the KO compared to WT mice. Microglia were also isolated from the brain, and the proteome was analyzed by liquid chromatography mass spectrometry.

2020-06-29 | PXD015939 | Pride

Global transcriptome profiling was performed for keratinocytes transfected with either miR-146a mimics (Pre-146a) or negative control (Pre-NC).

Project description:To find out potiential target gene of miR-146a,we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to target miR-146a. Human keratinocytes was transfected with either miR-146a mimics (Pre-146a) or negative control (Pre-NC) for 48h, then RNA was extracted for whole genome microarray expression profiling.

2019-02-07 | GSE126137 | GEO

A transgenic mouse model for early prostate metastasis to lymph nodes.

Project description:The emergence of recurrent, metastatic prostate cancer following the failure of androgen-deprivation therapy represents the lethal phenotype of this disease. However, little is known regarding the genes and pathways that regulate this metastatic process, and moreover, it is unclear whether metastasis is an early or late event. The individual genetic loss of the metastasis suppressor, SSeCKS/Gravin/AKAP12 or Rb, genes that are downregulated or deleted in human prostate cancer, results in prostatic hyperplasia. Here, we show that the combined loss of Akap12 and Rb results in prostatic intraepithelial neoplasia (PIN) that fails to progress to malignancy after 18 months. Strikingly, 83% of mice with PIN lesions exhibited metastases to draining lymph nodes, marked by relatively differentiated tumor cells expressing markers of basal (p63, cytokeratin 14) and luminal (cytokeratin 8 and androgen receptor) epithelial cells, although none expressed the basal marker, cytokeratin 5. The finding that PIN lesions contain increased numbers of p63/AR-positive, cytokeratin 5-negative basal cells compared with WT or Akap12-/- prostate lobes suggests that these transitional cells may be the source of the lymph node metastases. Taken together, these data suggest that in the context of Rb loss, Akap12 suppresses the oncogenic proliferation and early metastatic spread of basal-luminal prostate tumor cells.

| S-EPMC3916780 | biostudies-literature

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