Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA186802 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiles of kidneys that underwent reversible UUO model using model mice for erythropoietin-deficiency anemia (ISAM)
| PRJNA193435 | ENA
Project description:We established a novel mouse model for postnatal erythropoietin (Epo)-deficiency anaemia, designated ISAM (inherited super anemic mouse), using a transgenic complementation rescue technique. To identify Epo-regulated genes in vivo, we examined the mRNA expression profile in the bone marrow of ISAM 6 hours after recombinant human EPO (rHuEPO) administration. Erythropoietin-induced gene expression in mouse bone marrow was measured at 6 hours after rHuEPO administration (3,000 U/kg). Three Epo-treated samples were analyzed, and two PBS-treated and one untreated samples were used as a control group.
2013-01-18 | E-GEOD-43585 | biostudies-arrayexpress
Project description:We established a novel mouse model for postnatal erythropoietin (Epo)-deficiency anaemia, designated ISAM (inherited super anemic mouse), using a transgenic complementation rescue technique. To identify Epo-regulated genes in vivo, we examined the mRNA expression profile in the bone marrow of ISAM 6 hours after recombinant human EPO (rHuEPO) administration.
2013-01-18 | GSE43585 | GEO
Project description:The mechanism underlying thrombocytosis in patients with iron deficiency anemia remains unknown. We present findings that support the hypothesis that low iron biases the commitment of Megakaryocytic-Erythroid Progenitors (MEP) toward the megakaryocytic (Mk) lineage in mice. In MEP of Transmembrane serine protease 6 knockout (Tmprss6-/-) mice, which exhibit iron deficiency microcytic anemia concomitant with thrombocytosis, we observed a megakaryocytic (Mk) bias, decreased labile iron, and decreased proliferation relative to wild-type (WT) MEP. Bone marrow transplantation assays suggest that the systemic iron deficiency of the Tmprss6-/- recipients contributes to the MEP lineage commitment bias. Genes involved in metabolic, VEGF, and ERK pathways were enriched among those differentially expressed between WT and Tmprss6-/- MEP. Corroborating our findings from the murine model of chronic iron deficiency anemia, primary human MEP also exhibited decreased proliferation and Mk-biased commitment when their iron sensing pathways were disrupted by knockdown of Transferrin Receptor 2. These data are consistent with a model in which low iron in the marrow environment affects MEP metabolism, attenuates ERK signaling, slows proliferation, and biases MEP toward Mk lineage commitment. Keywords: megakaryocytic-erythroid progenitor (MEP), iron deficiency, Tmprss6
2023-03-17 | GSE227563 | GEO
Project description:ATAC-seq profiling of Nfat5 KO and wild type macrophages derived from bone marrow (primary cells), treated or not with Lipopolysaccharide (LPS).
2021-06-09 | GSE111476 | GEO
Project description:TH-MYCN Mice with Caspase-8 Deficiency Develop Advanced Neuroblastoma with Bone Marrow Metastasis
| PRJNA182245 | ENA
Project description:TH-MYCN Mice with Caspase-8 Deficiency Develop Advanced Neuroblastoma with Bone Marrow Metastasis
| PRJNA179446 | ENA
Project description:To comprehensively understand how dendritic cells (DCs) are reprogrammed by lung fibroblasts- and their derived COX-2/PGE2, we employed lung fibroblasts isolated from WT or Ptgs2-/- mice, and collect their conditioned medium (CM) to stimulate the ex vivo cultured bone marrow (BM)-derived DCs (BM-DCs), with the PGE2 treatment as a control. After the treatment, BM-DCs were harvested for RNA extraction and the transcriptional profiles were analyzed by RNA sequencing (RNA-seq).
2022-07-19 | E-MTAB-11873 | biostudies-arrayexpress
Project description:Diamond-Blackfan anemia (DBA) is characterized by anemia and cancer susceptibility, and is caused by mutations in ribosomal genes, including Rpl11. Here, we report that Rpl11-heterozygous embryos are not viable, and homozygous deletion of Rpl11 in adult mice results in death within a few weeks, accompanied by bone marrow aplasia and intestinal atrophy. Importantly, deletion of a single Rpl11 allele in adult mice results in anemia associated to decreased erythroid progenitors and defective erythroid maturation. These phenotypes are also present in mice transplanted with inducible heterozygous Rpl11 bone marrow, indicating a cell-autonomous role of RPL11 in erythropoiesis. Additionally, fibroblasts lacking one or both Rpl11 alleles show defective p53 activation upon ribosomal stress or DNA damage. Furthermore, fibroblasts and hematopoietic tissues from heterozygous Rpl11 mice present higher basal cMYC levels. Accordingly, heterozygous Rpl11 mice are highly susceptible to radiation-induced lymphomagenesis. We conclude that Rpl11-deficient mice recapitulate DBA disorder, including cancer predisposition. RNAseq profiles of bone marrow hematopoietic progenitors cells from WT (Rpl11+/+:: Tg.UbC-CreERT2) and LOX (Rpl11+/lox::Tb.Ub-CreERT2) mice, n=4 independent animals per genotype
2015-09-01 | E-GEOD-72537 | biostudies-arrayexpress
Project description:Mature blood cells are produced continuously from hematopoietic stem and progenitor cells (HSPCs) in the bone marrow (BM). During chronic inflammation, this process may be perturbed by inflammatory cytokines acting on HSPCs to cause anemia of inflammatory disease. Among BM HSPCs, we found the receptor for interleukin (IL)-33, ST2, was expressed preferentially and highly on erythroid progenitors. Induction of inflammatory spondyloarthritis in mice increased IL-33 in BM plasma, and IL-33 was required for inflammation-dependent suppression of erythropoiesis in BM. Conversely, administration of IL-33 in healthy mice suppressed erythropoiesis, decreased hemoglobin expression, and caused anemia. Using purified erythroid progenitors in vitro, we showed that IL-33 directly inhibited terminal maturation. This effect was dependent on NF-kB activation and was associated with altered signalling events downstream of the erythropoietin receptor. Accordingly, IL-33 also suppressed erythropoietin-induced stress erythropoiesis in vivo. These results reveal a role for IL-33 in regulation of erythropoiesis during inflammatory disease and define a new target for its treatment.
2020-05-15 | GSE141480 | GEO