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Small RNAseq in donor BMDCs and BMDCs that received exosomes

ABSTRACT: small RNAseq was preformed on Wt bone marrow-derived dendritic cells (BMDC) and miR-155 and miR-146a double knockout (DKO) BMDCs that received Wt exosomes to investigate the differences in transferred miRNA

ORGANISM(S): Mus musculus

PROVIDER: GSE67946 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA281344

REPOSITORIES: GEO

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small RNAseq in donor BMDCs and BMDCs that received exosomes

Project description:small RNAseq was preformed on Wt bone marrow-derived dendritic cells (BMDC) and miR-155 and miR-146a double knockout (DKO) BMDCs that received Wt exosomes to investigate the differences in transferred miRNA Small RNA profiles were generated from Wt donor BMDCs and DKO BMDCs given Wt exosomes 3 replicates in each group

2016-07-03 | E-GEOD-67946 | biostudies-arrayexpress

Gene profile of aged Wt, miR-155-/-, miR-146a-/- and DKO CD4+ T cells

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Gene expression profiling in wild-type, Irf5-KO, Lyn-KO and Lyn/Irf5-DKO BMDCs unstimulated or stimulated with CpG-B ODN

Project description:To characterize the relationship between IRF5 and Lyn in innate immune responses at a genome-wide scale, we performed gene expression microarray analysis for wild-type (WT), Irf5-KO, Lyn-KO and Lyn/Irf5-DKO bone marrow-derived dendritic cells (BMDCs) with or without 6 h-stimulation with 150 nM CpG-B ODN. We extracted the transcripts that were upregulated by CpG-B ODN in WT BMDCs, further upregulated in Lyn-KO BMDCs and then downregulated in Lyn/Irf5-DKO BMDCs (fold change â?¥ 2, false discovery rate < 0.05). When these 79 transcripts were sorted by their expression levels in Lyn-KO BMDCs, most of the top 20 genes (13 out of 20) were those encoding type I interferons (IFNs), indicating that Lyn particularly suppresses IRF5 induction of type I IFNs. BMDCs from WT, Irf5-KO, Lyn-KO and Lyn/Irf5-DKO mice in a C57BL/6 background were unstimulated or stimulated with CpG-B ODN. Biological triplicate for each genotype were analyzed (24 samples in total).

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Gene expression profiling in wild-type, Irf5-KO, Lyn-KO and Lyn/Irf5-DKO BMDCs unstimulated or stimulated with CpG-B ODN

Project description:To characterize the relationship between IRF5 and Lyn in innate immune responses at a genome-wide scale, we performed gene expression microarray analysis for wild-type (WT), Irf5-KO, Lyn-KO and Lyn/Irf5-DKO bone marrow-derived dendritic cells (BMDCs) with or without 6 h-stimulation with 150 nM CpG-B ODN. We extracted the transcripts that were upregulated by CpG-B ODN in WT BMDCs, further upregulated in Lyn-KO BMDCs and then downregulated in Lyn/Irf5-DKO BMDCs (fold change ≥ 2, false discovery rate < 0.05). When these 79 transcripts were sorted by their expression levels in Lyn-KO BMDCs, most of the top 20 genes (13 out of 20) were those encoding type I interferons (IFNs), indicating that Lyn particularly suppresses IRF5 induction of type I IFNs.

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

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Project description:Gene profile of aged Wt, miR-155-/-, miR-146a-/- and DKO CD4+ T cells

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Epistasis between TIFAB and miR-146a, neighboring genes in del(5q) MDS

Project description:Interstitial deletion of a single copy of chromosome 5q is the most frequent cytogenetic alteration in Myelodysplastic Syndromes (MDS), which results in reduced dosage of numerous genes. Furthermore, the extent of the 5q deletion determines disease severity, suggesting cooperation between deleted genes in the proximal and distal regions of del(5q). Although the contribution of individual genes to the pathogenesis of del(5q) MDS has been investigated, less is known about the epistatic interactions and/or cooperation between neighboring deleted genes. Deletion of TRAF-interacting protein with forkhead-associated domain B (TIFAB) and miR-146a, two haploinsufficient genes in del(5q) MDS, has been previously reported to activate the Toll-like receptor (TLR) signaling cascade in hematopoietic stem/progenitor cells (HSPC) by increasing TRAF6 protein stability and mRNA translation, respectively. To investigate the epistasis of TIFAB and miR-146a, we generated a mouse model in which Tifab and miR-146a were simultaneously deleted (Tifab-/-;miR-146a-/-, dKO). Herein, we report that combined hematopoietic-specific deletion of Tifab and miR-146a results in more rapid and severe cytopenia, and progression to a fatal bone marrow (BM) failure-like disease as compared to Tifab- or miR-146adeficiency alone. HSPC from Tifab-/-, miR-146a-/-, and dKO mice exhibit enrichment of gene 69 regulatory networks associated with innate immune signaling. Moreover, a subset of the differentially expressed genes is controlled synergistically following deletion of Tifab and miR-146a. Notably, nearly half of these defined synergy response genes identified in the mouse models were aberrantly expressed in del(5q) MDS HSPC when TIFAB (5q31) and miR-146a (5q33.3) were both deleted. Thus, synergistic control of gene expression following deletion of epistatic haploinsufficient genes in del(5q) MDS may be an underlying mechanism of the diseased state.

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