Transcription profiling of bone marrow derived cells from mice stimulated with RANKL to generate osteoclasts in a time series
ABSTRACT: Bone marrow derived cells stimulated with RANKL (receptor activator of nuclear factor kappa B ligand, also known as Tumor necrosis factor ligand superfamily member 11) to generate osteoclasts.
Developmental dynamics : an official publication of the American Association of Anatomists 20070801 8
Osteoclasts are bone-resorbing cells derived from the myeloid lineage that play a central role in bone remodeling and inflammatory bone erosion diseases. The receptor activator of NF-kappaB ligand (RANKL) produced by osteoblasts and activated immune cells initiates the development of osteoclasts in the bone marrow. Using time series gene expression data, the intrinsic processes and the extrinsic factors that control osteoclastogenesis were identified. The gene expression profiles display distinc ...[more]
Project description:The archetypal Th2 cytokine interleukin 4 (IL-4) has previously been shown to alternatively activate dendritic cells (DCs) both in vitro and in vivo.To more fully understand the impact of IL-4 dependent alternative activation of DCs, we used mRNA microarrays to define their transcriptional profile. RNAs were extracted from bone marrow-derived dendritic cells (BMDCs). Two groups of samples were taken, with three biological replicates in each: control untreated, and treated with recombinant-IL4 (at 20 ng/ml).
Project description:We sequenced microRNAs from bone marrow derived macrophages derived from the control (WT) and RBP-J conditional knockout mice (RBP-J KO; Rbpjf/f; LysM Cre). Examination of differential microRNA expression levels induced by TNF as well as regulated by RBP-J in bone marrow derived macrophages.
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Project description:The Mouse Promylocyte (MPRO) cell line was induced to differentiate over four days during which time MYC expression decreases. MYC is required for rDNA transcription; by looking at global gene expression under these conditions, our aim was to correlate the expression of Pol I related/specific genes with that of MYC as well as contrast to those genes specific to Pol II and III transcription.
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Project description:Epigenetic regulation is a fundamental mechanism mediating various cellular processes. However, epigenetic mechanisms in osteoclastogenesis remain to be elucidated. We performed microarray analysis to investigate gene expression in osteoclasts derived from wild-type and Dnmt3aknockout mice. In vitro osteoclast culture were performed using wild-type control and Dnmt3a knockout bone marrow-derived monocyte/macrophage precursor cells.
Project description:Inflammation is a hallmark of multiple disease processes, including inflammatory bowel disease (IBD). The transcription factor NF-kappaB plays a critical role in this response through its effects on pro-inflammatory gene expression. Consequently, homeostatic mechanisms that control NF-kappaB activity have been found to play important roles in controlling inflammatory responses in physiologic and pathologic states. Copper Metabolism Murr1 Domain containing 1 (COMMD1), a regulator of copper excretion and other transport pathways, has been shown to play a role in limiting NF-kappaB activation. However, it remains unclear if this factor plays a necessary role in the control of inflammation or in the pathogenesis of inflammatory disorders in vivo. Using a myeloid-cell specific model of Commd1 deficiency in mice we evaluated the contribution of this factor to inflammatory responses. We found that this gene plays an important role as a negative regulator of the LPS transcriptional response, and deficiency in this factor led to sensitization to in vivo models of sepsis. In addition, we identified single nucleotide variants located near COMMD1 that are associated with decreased expression of this gene in humans. Interestingly, these polymorphisms also show a suggestive association signal with ulcerative colitis risk. Consistent with the possibility that genetic variation in COMMD1 expression may predispose to colitis, we find that myeloid deletion of Commd1 leads to more severe colonic inflammation and cancer progression in experimental colitis models. Altogether, the data support the notion that COMMD1 expression in myeloid cells plays an important anti-inflammatory role in physiologic states and human disease. Bone marrow derived macrophages (BMDM) were isolated from two individual wildtype - and two Commd1 knockout mice. Cells from individual mice were splitted and were treated with LPS for 3h, 24h, or, were left untreated. The corresponding 12 cell samples were subjected to total RNA preparation and subsequently used for Single-Color-based Microarray Analysis (Agilent Technologies).
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