Next generation sequencing of neutrophils from WT, PyMT and PyMT-Cxcr2-/- mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA691913 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report the comparison of gene expression of neutrophils in the mammary gland of PyMT and PyMT-Cxcr2-/- animals as well as the one of WT bone marrow
2021-05-21 | GSE164766 | GEO
Project description:We report the comparison of gene expression of neutrophils in the spleen of WT and -Cxcr2-/- animals
2022-09-29 | GSE209860 | GEO
Project description:[Background] TNFa-induced adipose-related protein (TIARP) is a six-transmembrane protein that is expressed on macrophages, neutrophils and synoviocytes. We have recently reported that TIARP deficient mice (TIARP-/-) spontaneously developed arthritis, and had the high susceptibility to collagen-induced arthritis (CIA) with enhanced interleukin (IL)-6 production. However, the effect of TIARP to neutrophils and fibroblast-like syonoviocytes (FLS) has not been clearly elucidated. [Methods] We analyzed the roles of TIARP in K/BxN serum transfer model using TIARP-/- mice. We characterized the differences of neutrophils between WT and TIARP-/- mice by DNA microarray. Transmigration assays of TIARP-/- neutrophils were performed in vitro and in vivo. FLS were cultured with TNF? and the production of CXCL2 (a specific ligand of CXCR1 and CXCR2) and IL-6 were measured by ELISA. Moreover, TIARP-/- mice transferred with K/BxN serum were treated with anti-IL-6R antibodies. [Results] Arthritis in TIARP-/- mice transferred with K/BxN serum was significantly exacerbated. We identified overexpression of CXCR1 and CXCR2 in TIARP-/- neutrophils by DNA microarray. Neutrophils from TIARP-/- mice showed strong migration activity. The enhancement of chomotactic activity of TIARP-/- neutrophil was greatly facilitated by CXCL2 in vitro and in vivo. In addition, TIARP-/-FLS has enhanced the production of CXCL2 and IL-6 and the cell proliferation in the presence of TNFa, and the blockade of IL-6R significantly attenuated arthritis in vivo. [Conclusion] Our findings indicate that TIARP might down-regulate the production of CXCL2 and IL-6 in FLS, and the expression of chemokine receptors (CXCR1 and CXCR2) in neutrophils, resulting in the protective ability of neutrophils migration into arthritic joints. Mice were treated with thiogycollate medium intraperitoneally. After 3 days, peritoneal macrophages were isolated from three WT or TIARP-deficient mice, and these cells were stimulated by TNF? for 24 hours. Ly6G+ Neutrophils were isolated from splenocytes by MACS.
2015-09-23 | E-GEOD-73306 | biostudies-arrayexpress
Project description:To investigate the role of DREAM (a transcriptional repressor) in regulating gene transcription in neutrophils under inflammatory conditions, we conducted the next generation sequencing using unstimulated and TNF-alpha-stimulated neutrophils isolated from WT and DREAM KO mice.
2021-11-03 | GSE172394 | GEO
Project description:[Background] TNFa-induced adipose-related protein (TIARP) is a six-transmembrane protein that is expressed on macrophages, neutrophils and synoviocytes. We have recently reported that TIARP deficient mice (TIARP-/-) spontaneously developed arthritis, and had the high susceptibility to collagen-induced arthritis (CIA) with enhanced interleukin (IL)-6 production. However, the effect of TIARP to neutrophils and fibroblast-like syonoviocytes (FLS) has not been clearly elucidated. [Methods] We analyzed the roles of TIARP in K/BxN serum transfer model using TIARP-/- mice. We characterized the differences of neutrophils between WT and TIARP-/- mice by DNA microarray. Transmigration assays of TIARP-/- neutrophils were performed in vitro and in vivo. FLS were cultured with TNFα and the production of CXCL2 (a specific ligand of CXCR1 and CXCR2) and IL-6 were measured by ELISA. Moreover, TIARP-/- mice transferred with K/BxN serum were treated with anti-IL-6R antibodies. [Results] Arthritis in TIARP-/- mice transferred with K/BxN serum was significantly exacerbated. We identified overexpression of CXCR1 and CXCR2 in TIARP-/- neutrophils by DNA microarray. Neutrophils from TIARP-/- mice showed strong migration activity. The enhancement of chomotactic activity of TIARP-/- neutrophil was greatly facilitated by CXCL2 in vitro and in vivo. In addition, TIARP-/-FLS has enhanced the production of CXCL2 and IL-6 and the cell proliferation in the presence of TNFa, and the blockade of IL-6R significantly attenuated arthritis in vivo. [Conclusion] Our findings indicate that TIARP might down-regulate the production of CXCL2 and IL-6 in FLS, and the expression of chemokine receptors (CXCR1 and CXCR2) in neutrophils, resulting in the protective ability of neutrophils migration into arthritic joints.
2015-09-23 | GSE73306 | GEO
Project description:By performing transcriptome-wide RNA sequencing (RNA-seq) analysis on the peritoneal neutrophils from Alkbh5-deficient mice (Alkbh5-/-) and Wild-type littermates (Alkbh5+/+) at 12h or 36h after mild cecal ligation and puncture (CLP), respectively, we want to identify potential targets of ALKBH5 and characterize the transcriptional landscape in neutrophils during antibacterial innate defense. Gene Ontology biological processes enrichment analysis of the significantly differentially expressed genes (DEGs) showed that neutrophil migration made up the most significantly enriched biological processes with annotations of neutrophil association upon loss of ALKBH5 in neutrophils, at both 12h and 36h after CLP. Many significantly DEGs also encompassed transcriptional signatures related to neutrophils, specifically to neutrophil influx into the infection site, including chemotaxis, response to chemokine, extravasation, ERK1 and ERK2 cascade, homeostasis of neutrophils. ALKBH5 deletion led to significantly decreased transcript expression of neutrophil migration-promoting Cxcr2 and Nlrp12; while increased transcript expression of neutrophil migration-suppressive Ptger4, Tnc, and Wnk1. These results demonstrated that ALKBH5 imprints migration-promoting transcriptional landscape in neutrophils to enable their migration into the site of infection for antibacterial innate defense.
2022-05-24 | GSE198316 | GEO
Project description:Atglflox/flox (B6N.129S-Pnpla2tm1Eek/J), S100A8-cre+/- (B6.Cg-Tg(S100A8-cre,-EGFP)1Ilw/J) mice were obtained from The Jackson Laboratory. Atglflox/flox mice were bred to S100A8-cre+/- mice to generate Atglflox/WTS100A8-cre+/- mice, which were backcrossed onto Atglflox/flox mice to generate Atglflox/floxS100A8-cre+/- mice (Atgl neutrophils-specific knock out, Atgl-cKO). Age-matched littermate Atglflox/flox mice were used as wild-type (WT) controls. To compare of the gene expression of the lung-infiltrating neutrophils isolated from Atgl-cKO mice and their WT littermates, AT3-g-csf cells were injected into the fourth mammary fat pads of female WT and Atgl-cKO mice (10-week-old, n = 4/group). The AT3-g-csf cell line is based on a murine breast cancer cell line (AT3) derived from MMTV-PyMT tumors in the C57BL/6 background, and further constructed to overexpress granulocyte-colony stimulating factor (G-CSF) for induction of the host inflammatory condition. At day 10 (pre-metastatic stage), the mice were euthanized and then Ly6G+ neutrophils were isolated from lung by using anti-Ly6G MicroBead Kit (Miltenyi Biotec) following manufacturer’s instructions. The isolated neutrophils were analyzed by flow cytometry and the cells with a > 95% purity were used for the next procedure. Total RNA was isolated from neutrophils using the miRNeasy Mini kit (Qiagen) and the transcriptional profiles of neutrophils were analyzed by RNA sequencing.
2020-06-28 | E-MTAB-9235 | biostudies-arrayexpress
Project description:We report the comparison of gene expression in the mammary gland and pituitary of WT Balb and CXCR2 KO balb animals which were housed in conventional or SOPF conditions
2020-02-05 | GSE144231 | GEO
Project description:Previously, lncRNA Malat1 knockout mice were generated by insertional inactivation. By crossing this line to MMTV-PyMT mammary tumor mouse model, we produced PyMT;Malat1 wild-type (WT) and PyMT;Malat1 knockout (KO). Furthermore, we generated Malat1 transgenic mice by targeting ROSA26 locus and bred them to PyMT;Malat1 knockout mice to produce Malat1-rescued PyMT;Malat1 knockout;Malat1 transgenic animals (TG). Using mammary tumors from the three groups of animals, we performed RNA-Seq analysis to identify differentially up-regulated genes in KO tumors to find novel target genes of YAP-TEAD pathway.
2018-09-18 | GSE110239 | GEO
Project description:Next generation sequencing of unstimulated and TNF-alpha-stimulated WT and DREAM-null neutrophils
| PRJNA723207 | ENA