Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA170917 | ENA |
REPOSITORIES: ENA
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Project description:The involvement of mature hematopoietic cells in disease pathogenesis is well recognized. However it is not clear how if and how primitive progenitors might contribute to inflammatory disease processes. This microarray experiment is used together with data from functional assays to determine how primitive progenitors are altered in a mouse model of autoimmune arthritis and how this in turn might contribute to the disease process. KSL cells were FACS sorted from 7 to 9 6-7 week old arthritic (KRNxG7) mice as well as from two strains of non-arthritic age-matched control mice: KRN and B6xG7 mice. Cells were sorted using identical conditions and identical sorting gates. To verify the primitive status of the KSL cells, Lin+ cells were also MACS sorted from these same mice. All the mice used in this study were C57BL/6 background strain. G7 mice are congenic with C57BL/6 but with MHC II I-Ab replaced with MHC II I-Ag7.
2012-12-31 | E-GEOD-39458 | biostudies-arrayexpress
Project description:Runx/Cbfb heterodimers play important roles in the development of hematopoietic cells in mouse embryos and adults. In order to identify genes that are regulated by Runx/Cbfb, we purified Lin– c-kit+ Sca1+ (LSK) cells and Lin– c-kit+ Sca1– CD16/32+ (GMP) cells from Vav1-iCre x Cbfb(F/F) and Vav1-iCre x Cbfb(F/+) mice and profiled gene expression using microarray.
2014-04-05 | GSE55227 | GEO
Project description:We report a genome-wide microarray analysis of gene expression in mouse embryonic stem cell (ESC) and in vitro ES-derived cells. iHoxB4 ESCs were transduced with a library of shRNAs targeting >15,000 genes, and were differentiated towards hematopoietic stem and progenitor cells by forcing HoxB4 expression in the cells. Five cell populations were isolated on differentiation days 6 and 20. Differentiated mesodermal/endothelium cell population D6F (Ssea1-Flkl+Cxcr4-), endodermal cell population D6C (Ssea1-Flkl-Cxcr4+), D20LS (Lin-Sca1+c-Kit–), D20LK (Lin–Sca1–c-Kit+), and D20LSK (Lin–Sca1+c-Kit+) cells were purified by FACS. Transduced iHoxB4 cells were analyzed as undifferentiated control cells. The experiment was performed three times independently.
2016-12-31 | GSE86853 | GEO
Project description:Expression data from cultured c-Kit+Sca-1+Lin- (KSL)cells
| PRJNA169919 | ENA
Project description:Precise study of HSCs during regeneration has been impeded by the rarity of the HSC population and depletion of phenotypic HSCs early following genotoxic stresses, such as total body irradiation (TBI). We isolated bone marrow (BM) ckit+sca-1+lin- (KSL) cells, which are enriched for HSCs, from adult C57Bl6 mice before and at several time points following TBI, as a means to map the dynamic molecular response of HSC regeneration. We isolated BM KSL cells and myeloid progenitor cells (c-kit+sca-1-lin- cells) at day +14 after irradiation and compared the gene expression profile of regenerating HSCs versus steady state HSCs (non-irradiated) and committed progenitor cells.
2016-04-05 | E-GEOD-79744 | biostudies-arrayexpress
Project description:To understand molecular mechanisms that are deregulated in hematopoietic stem progenitor cells from transgenic mice that express the constitutively active form of IKK2 protein in HSCs (CA/CA mice), we isolated Flt3 low Lin-Sca1+c-Kit+ (LSK) cells from control and CA/CA mice and performed microarray analysis using the Illumina's MouseWG-6 v2.0 Expression BeadChip platform.
2018-10-13 | GSE121195 | GEO
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.
2021-01-26 | PXD010486 | Pride
Project description:We used Fancd2-/- mice to understand its mechanism of action. Transcriptome analysis of cKit+ Sca1+ Lin- (KSL) cells discovered that only four genes changed their expression levels significantly after chronic OXM administration in both Fancd2−/− and wild-type mice: mKi67 and Cenpf were up-regualted by 1.4 fold; Spp1 and Oasl2 were significantly down-regulated by 10.5 and 1.5 fold, respectively. Both mKi67 and Cenpf genes are cell cycle-regulated genes and proliferation markers. Their up-regulation was consistent with our observation in flow cytometry analysis that oxymetholone stimulated the proliferation of hematopoietic stem and progenitor cells. RNAseq analysis showed no effects on mTert mRNA expression with chronic androgen therapy, but instead suggested down-regulation of Spp1 and Oasl2 as an important mechanism for the drug’s action. Our RNAseq analysis also revealed that Fancd2−/− KSL cells showed clear changes in mRNA expression profiles compared to wild-type controls: 430 genes were down-regulated by more than 1.5 fold, whereas 159 genes were up-regulated. Gene ontology analysis revealed key pathways to be significantly altered in Fancd2−/− KSL cells. Besides the abnormal cell cycle status expected from our earlier flow cytometry analysis, surprisingly we noticed that a group of genes involved in immune responses and inflammation, comprising Cfp (Properdin), Socs2, Ccr1, Ccr2, Ccr5, Chga (Chromogranin A), Ifi30 (Interferon Gamma-Inducible Protein 30), Lgmn, Txn, and Sell (selectin L), were up-regulated in Fancd2−/− KSL cells. We therefore hypothesize that some genes up-regulated in FA HSPCs may be part of an innate immune response to DNA damage. In addition, whole bone marrow cells were also analyzed in parallel with KSL cells. As compared to whole bone marrow cells, the genes enriched in KSL cells in wild-type mice were listed in details in the corresponding publication. This information can be a good resource for the future gene expression analysis of HSPCs. Finally, we compared the gene expression profiles of early progenitors between OXM-treated and placebo-treated mice. There were no significant differences at all in gene expression between OXM-treated wild-type erythroid progenitors and their placebo-treated wild-type counterparts, with no genes displaying an expression change higher than 1.2 fold. Importantly, no up-regulation of EPO-inducible genes such as Socs1, Socs2, Socs3, and Cish was seen in wild-type mice treated with OXM. Furthermore, there was no differential expression of the well-known EPO target transferrin receptor or any other major players of the Epo-R signaling network such as Bcl2l1, Cdc25a, Btg3, Ccnd2, Lyl1, Pim3, and Tnfrsf13c. These results indicate that EPO might not play a role in the action of OXM in the erythroid lineage. The goal of this study is to investigate gene expression changes in Fancd2 knockout mice in response to oxymetholone treatment. The study focuses on two bone marrow cell populations: cKit+ Sca1+ Lin- cells (representing hematopoietic stem and progenitor cells) and Ter119+/CD71high/FSChigh cells (representing proerythroblasts and basophilic erythroblasts). Both populations were sorted twice by FACS to ensure the purity. Cells of interest were collected in Trizol and RNA was isolated using RNAeasy mini prep kit. mRNAs were positively selected using oligo(dT)- Dynobeads and treated with DNase I. RNAseq libraries were then constructed using Illumina TruSeq RNA Sample Prep Kit and sequenced as 51 base-length reads on an Illumina HiSeq 2000 genome analyzer. For KSL libraries, each sample represented total mRNA isolated from pooled KSL cells of 5 individual mice; for basophilic erythroblast libraries, each library represented total mRNA isolated from basophilic erythroblasts of one individual mouse; for whole bone marrow libraries, each sample represented a combined library originally from 5 individual mice. All reads were mapped to the mouse reference genome (version mm9) using Bowtie short read aligner software (http://bowtie-bio.sf.net). Most of the data analysis was performed using EdgeR GLM algorithms. For the comparison of oxymetholone KSL libraries vs placebo KSL libraries, more stringent pair-wise comparisons were used to keep a consistent flow cytometric setting among each pair. The common gene list was the one shared by all three comparisons: COM17 vs HSC_101b, HSC_13 vs HSC_18, and HSC_23 vs QZ_35 for Fancd2−/− KSL cells; HSC_3 vs QZ_36, HSC_22 vs HSC_24, and COM15 vs COM16 for wild-type KSL cells. Data-mining and pathway analysis were carried out with the MetaCore integrated software suite (Thomson Reuters, New York, USA).
2015-01-06 | E-GEOD-58724 | biostudies-arrayexpress