Project description:Murine bone marrow CD55+ myeloid progenitors were fixed and submitted to Flex ScRNA-seq with CITE-seq in order to investigate eosinophil ontogeny and development.
Project description:6-plex TMT LC-MSMS quantification of proteins in myeloid progenitors (Lineage- Sca1- Kit+ cells) isolated from the bone marrow of 8-12 week old male and female control and Elp3-deficient (Elp3fl/fl vav-iCreT/+) mice. Biological triplicates of each genotype were analyzed, each consisting of 1.10e6 cells from pools of 12-14 control (Elp3fl/fl) or 26-38 (Elp3-deficient) male and female mice.
Project description:The TLR9-/- mice had more myeloid cells and progenitors and fewer B cells in the bone marrow. Activity of Fos and Cebpb, important mediator of myelopoiesis, in the cluster of HSPCs were increased. PU.1 and Fos, critical transcription factors mediating osteoclastogenesis, were upregulated in monocyte progenitors. In addition to myeloid biased hematopoiesis in TLR9-/- mice, there were upregulated levels of inflammatory cytokines in the TLR9-/- bone marrow.
Project description:Compared gene expression between Lin-Sca1-cKit+ myeloid progenitors isolated from the bone marrow of 6-8 week old wildtype and Mirc11-/- mice. Previously observed that overexpression of Mirc11 in hematopoietic progenitors increased myeloid differentiation whereas loss of Mirc11 decreased myeloid differentiation. Performed RNA-seq to identify potential genes involved in myeloid differentiation regulated by Mirc11. Gene expression analysis of Mirc11 deficient myeloid progenitors revealed a decrease in Toll like receptor and interferon signaling. This anti-inflammatory phenotype was further observed in mature cells as Mirc11-/- bone marrow derived macrophages (BMDMs) have an attenuated response to inflammatory lip-opolysaccharide (LPS).
Project description:To investigate the role of FoxO transcription factors as mediators of hematopoietic stem cell resistance to oxidative stress. Experiment Overall Design: Study the effect of the deficiency of FoxO1, FoxO3, and FoxO4 in murine bone marrow hematopoietic stem cells and myeloid progenitors on expression of genes involved in reactive oxygen species (ROS) metabolism.