Project description:The microarray analysis is to investigate the different expression profile of microRNAs in bone marrow-derived progenitor cells from type 2 diabetic mice and healthy control mice. microRNA expression profiles were compared between bone marrow-derived progenitor cells from either type 2 diabetic db/db mice or their in-colony control litter db/+ mice.
Project description:The microarray analysis is to investigate the different expression profile of microRNAs in bone marrow-derived progenitor cells from type 2 diabetic mice and healthy control mice. microRNA expression profiles were compared between bone marrow-derived progenitor cells from either type 2 diabetic db/db mice or their in-colony control litter db/+ mice. Total RNA was extracted from bone marrow-derived progenitor cells from either type 2 diabetic db/db mice (Jackson lab, # 000642) or their in-colony control litter db/+ mice. N=3 per group.
Project description:We reported the function of Roquin-1 in the miRNA-sorting of macrophages derived exosomes. At first, we used the supernatant of 929 cells to culture the bone marrow derived macrophages (BMDM) from bone marrow cells of WT and Roquin-1 san:san mice. Then, we isolated the macrophages derived exosomes by ultracentrifugation. At last, we performed Next-generation sequencing to detect the differences of miRNA-sorting between WT and Roquin-1 macrophages derived exosomes.
Project description:Bone marrow-derived macrophages from mice were treated with recombinant Ssa1, a protein enriched in the hypoxic secretome of Candida albicans.
Project description:Macrophage dysfunction and polarization plays key role in chronic inflammation associated with diabetes and its complications. However, the effect of diabetes on macrophage transcriptome including long non-coding RNAs is not known. Here, we analyzed global changes in transcriptome of bone marrow macrophages isolated from type 2 diabetic db/db mice and control littermates db/+ mice using high throughput RNA-seq technique. Data analysis showed that expression of genes relevant to fibrosis, cell adhesion and inflammation were altered in diabetic db/db mice relative to control db/+ mice. Furthermore, expression of several known and novel long non coding RNAs and nearby genes was altered in db/db mice. Gene ontology and IPA showed activation of signaling netwroks relevant to fibrosis, cell adhesion and inflammatory pathways . This study for the first time demonstrated that diabetes profoundly affects macrophage transcriptome including expression of long non coding RNAs and altered the levels of genes relevant to diabetes complications. Bone marrow macrophages were isolated from 12 weeks old type 2 diabetic male db/db mice and control littermates db/+ mice. These were differentiated in culture for 7-8 days in the presence of 10 ng/ml of MCSF-1 (BMMC) or 20 ng/ml of GM-CSF (BMGM). Then RNA was extracted and used for RNA-seq.
Project description:Second dataset release from the Immunological Proteome Resource (ImmPRes). This dataset contains both lymphoid and myeloid populations. The whole list is as follows: Bone marrow derived eosinophils, bone marrow derived mast cells, bone marrow derived macrophages, NK cells, TH2 cells, TH17 cells, Cytotoxic T cells cultured in IL15 and Naive CD8+ T cells extractred from the lymph nodes of C57BL/6J mice.
Project description:To get insight into TRIM33 functions, TRIM33 ChIP-seq was carried out in murine macrophage cell line (RAW) and in bone marrow-derived macrophages (BMDM). The results showed that, in addition to its role in hematopoietic differentiation, TRIM33 may modulate PU.1 transcriptional activity during macrophage development and/or activation.To characterize the role of TRIM33 in macrophages, we bred TRIM33fl/fl mice with Lyz-Cre mice where the Cre recombinase gene is under the regulatory sequences of the Lyz gene that is expressed only in mature myeloid cells. Bone marrow cells from LyzCre/Trim33+/+ mice and LyzCre/Trim33flox/flox mice were differentiated in macrophages and treated during 0h, 4h, 12h and 24h with LPS. Using ChIP-seq, we provide a link between TRIM33 binding and H3K4me3 spreading on inflammatory genes in macrophages. Chromatin immunoprecipitations of TRIM33 and H3K4Me3 followed by multiparallel sequencing performed in murine bone marrow-derived macrophages (BMDM).