Project description:This study aims to identify miRNA molecules that are involved in inflammatory response in macrophages. A miRNA expression profiling of mouse macrophages comparing control wild type cells with DICER hypomorphic cells were conducted after these were subjected to treatment with LPS. Keywords: miRNA; DICER hypomorphic macrophages, microarray Pairwise comparison of Control versus DICER1 (Dcr1) hypomorphic cells. Two biological replicates were performed with three technical replicates for each biological replicate: 1 Control, 1 DICER1 (Dcr1) hypomorph, 2 treatment conditions. Exposed to LPS, harvested at 2hr and 4hr post treatment.
Project description:Transcriptional profiling of calpain-6-deficient murine bone marrow-derived macrophages comparing with calpain-6 wild-type macrophages. Total RNA was extracted from the pooled cells. Two-condition experiment, wild-type macrophages vs. calpain-6-deficiennt macrophages. The cells were derived from four mice, and were pooled for analysis.
Project description:Transcriptional profiling of calpain-6-deficient murine bone marrow-derived macrophages comparing with calpain-6 wild-type macrophages. Total RNA was extracted from the pooled cells.
Project description:Our systems analysis reported here demonstrates that TLR-responses in macrophages are markedly impaired by SHARPIN deficiency, and that SHARPIN controls expression of a subset of TLR2-induced, NF-kB and AP-1 dependent genes that overlaps with those affected by the hypomorphic panr2 mutation in NEMO. 46 total RNA samples from murine bone marrow derived macrophages were analyzed (32 by Agilent array, 14 by Affymetrix Exon array) On Agilent array, the responses of macrophages to 12hr stimulation with the TLR2 ligand PAM3CSK4 (300ng/mL) were analyzed in biological duplicates for five mutant mouse strains and respective controls: Sharpin(cpdm), Ikbkg(panr2), Atf3(KO), Il10(KO), and Nfkb1(KO).
Project description:Previous work has shown conflicting roles for Tec family kinases in regulation of Toll-like receptor (TLR)-dependent signalling in myeloid cells. In the present study, we performed a detailed investigation of the role of Btk and Tec kinases in regulating TLR signalling in several types of primary murine macrophages. We demonstrate that primary resident peritoneal macrophages deficient for Btk and Tec secrete less pro-inflammatory cytokines in response to TLR stimulation than wild type cells. In contrast, we found that bone marrow-derived and thioglycollate-elicited peritoneal macrophages deficient for Btk and Tec secrete more pro-inflammatory cytokines than wild type cells. We then compared the phosphoproteome regulated by Tec kinases and lipopolysaccharide in primary peritoneal and bone marrow derived macrophages. From this analysis we determined that Tec kinases regulate different signalling programs in these cell types. In additional studies using bone marrow-derived macrophages, we find that Tec and Btk promote phosphorylation events necessary for immunoreceptor-mediated inhibition of TLR signalling. Taken together, our results are consistent with a model where Tec kinases (Btk, Tec, Bmx) are required for TLR-dependent signalling in many types of myeloid cells. However, our data also support a cell type-specific TLR-inhibitory role for Btk and Tec that is mediated by immunoreceptor activation and signalling via PI3K.
Project description:Analysis of mRNA-seq of wild type bone marrow derived macrophages reveals how wild-type and Otud1 deficient bone marrow derived macrophages response to HSV-1 or SeV infection
Project description:To identify signaling pathways that are induced by macrophages infected with Histoplasma capsulatum, we examined the whole genome expression profile of murine bone marrow derived macrophages infected with conidia, the natural infectious particle of Histoplasma. Conidia induced the expression of signature Type I interferon response genes. The induction of a Type I interferon response was specific to conidia, yeast cells did not trigger the response. Macrophages that lack the Type I interferon receptor, IFNAR1, were infected and compared to wild-type macrophages. The expression of some Type I IFN response genes are dependent upon Keywords: Murine bone marrow derived macrophage transcriptional response to infection with Histoplasma capsulatum conidia We analyzed a series of 24 MEEBO arrays on which were hybed RNA amplified from bone marrow derived macrophages from C57BL/6 (WT) or ifnar1-/- mice either mock infected or infected with H. capsulatum conidia or yeast cells.
