Expression data comparing murine AE9a high and AE9a low expressing hematopoietic cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE84513 | GEO | 2016/07/19
SECONDARY ACCESSION(S): PRJNA329520
REPOSITORIES: GEO
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Project description:Microarray analysis was performed to examine potential differences in target gene expression of AE9a expressing low cells compared to AE9a expressing high cells. Potential contributing factors to AE9a induced leukemia were investigated. Embryonic day 13.5 to 14.5 fetal liver cells were harvested from C57Bl6 females. Cells were cultured in StemSpan media with 50ng/ml rat recombinant SCF, 10ng/ml human IL-6, and 10ng/ml murine IL-3. After overnight stimulation, cells were collected and transduced with two rounds of retrovirus (MIG-AE9a). Post transduction, cells were collected, counted and transplanted into lethally irradiated BoyJ recipient mice. Cells were expanded two to three weeks in vivo, mice were sacrificed, and bone marrow (BM) harvested. c-Kit+ cells were sorted (BD FACS Aria) for 30% low and 30% high GFP-expressing populations. Six AE9a low and six AE9a high samples were compared. RNA was isolated via the Qiagen RNeasy RNA isolation kit and submitted to the CCHMC Microarray Core. Samples were hybridized to an Affymetrix Mouse Gene 1.0 ST chip. Data was normalized using Expression Console and was analyzed using Qlucore Omics Explorer software.
2016-07-19 | E-GEOD-84513 | biostudies-arrayexpress
Project description:Fusion protein AML1-ETO resulted from t(8;21) translocation is highly related to leukemia development. We have previously shown that the expression of AE9a, a spliced form of AML1-ETO, can rapidly cause leukemia in mouse. To understand how AML1-ETO is involved in leukemia development, we used AE9a leukemia model to identify a novel AE9a interacting proteins PRMT1 (protein arginine methyltransferase 1) from primary leukemic cells expressing AE9a. To examine whether PRMT1 is involved in AE9a-mediated transcription regulation, genome wide gene expression analysis is carried out in hematopoietic cell line K562 (wild type or AE9a expressing) treated with (-) control siRNA or siPRMT1. Wild type or AE9a-expressing K562 cells with control siRNA or siPRMT1 in triplicate
2012-06-17 | E-GEOD-28135 | biostudies-arrayexpress
Project description:Fusion protein AML1-ETO resulted from t(8;21) translocation is highly related to leukemia development. We have previously shown that the expression of AE9a, a spliced form of AML1-ETO, can rapidly cause leukemia in mouse. To understand how AML1-ETO is involved in leukemia development, we used AE9a leukemia model to identify a novel AE9a interacting proteins PRMT1 (protein arginine methyltransferase 1) from primary leukemic cells expressing AE9a. To examine whether PRMT1 is involved in AE9a-mediated transcription regulation, genome wide gene expression analysis is carried out in hematopoietic cell line K562 (wild type or AE9a expressing) treated with (-) control siRNA or siPRMT1.
2012-06-18 | GSE28135 | GEO
Project description:We discovered a spontaneous differentiation path characterized by CD43 and c-Kit in the AE9a murine model, where the leukemia-initiating potential is lost while leukemic cells display features of erythroid maturation. Therefore, we sorted out CD43++c-Kit+, CD43+c-Kit- and CD43-c-Kit- AE9a leukemic cells for RNA-sequencing analyses to determine the underlying transcriptome.
2022-10-03 | GSE186040 | GEO
Project description:Expression data comparing murine AE9a high and AE9a low expressing hematopoietic cells
| PRJNA329520 | ENA
Project description:Purpose: Cholestatic liver injury is associated with intrahepatic biliary fibrosis, which can progress to cirrhosis. Resident hepatic progenitor cells (HPCs) expressing Prominin-1 (Prom1/CD133) become activated and participate in the expansion of cholangiocytes known as the ductular reaction. Previously, we demonstrated that in biliary atresia, Prom1(+) HPCs are present within developing fibrosis and that null mutation of Prom1 significantly abrogates fibrogenesis. Here, we hypothesized that these activated Prom1-expressing HPCs promote fibrogenesis in cholestatic liver injury. Methods: Using Prom1CreERT2-nLacZ/+;Rosa26Lsl-GFP/+ mice, we traced the fate of Prom1-expressing HPCs in the growth of the neonatal and adult livers and in biliary fibrosis induced by bile duct ligation (BDL). Results: Prom1-expressing cell lineage labeling with Green Fluorescent Protein (GFP) on postnatal day 1 exhibited an expanded population as well as bipotent differentiation potential towards both hepatocytes and cholangiocytes at postnatal day 35. However, in the adult liver, they lost hepatocyte differentiation potential. Upon cholestatic liver injury, adult Prom1-expressing HPCs gave rise to both PROM1(+) and PROM1(-) cholangiocytes contributing to ductular reaction without hepatocyte or myofibroblast differentiation. RNA-sequencing analysis of GFP(+) Prom1-expressing HPC lineage revealed a persistent cholangiocyte phenotype and evidence of Transforming Growth Factor-b pathway activation. Conclusion: Our data indicate that Prom1-expressing HPCs promote biliary fibrosis by activation of myofibroblasts in cholestatic liver injury.
2020-06-30 | GSE144726 | GEO
Project description:Combined gene expression and DNA occupancy profiling identifies JAK/STAT signaling as a valid therapeutic target of t(8;21) AML t(8;21) is commonly associated with acute myeloid leukemia (AML). The resulting AML1-ETO fusion proteins are involved in the pathogenesis of AML. To identify novel molecular and therapeutic targets, we performed combined gene expression and promoter occupancy profiling using a primary leukemia initiating cell-enriched population induced by AML1-ETO9a (AE9a). CD45, a negative regulator of cytokine/growth factor receptor and JAK/STAT signaling, is greatly downregulated; furthermore JAK1 and JAK2 are upregulated in these leukemia cells. Consequently, JAK/STAT signaling is enhanced in the AE9a leukemia cells. Importantly, AE9a leukemia cells are highly susceptible to perturbation of JAK/STAT signaling, and a JAK2-selective inhibitor, TG101209, effectively targets these leukemia cells in vivo, suggesting the potential efficacy of JAK2 inhibitors in treating t(8;21) AML. Wild-type or AE9a leukemic samples in triplicate.
2012-09-04 | E-GEOD-15195 | biostudies-arrayexpress
Project description:The transcriptomic differences between NRP2-high expressing and NRP2-low expressing cells in BT549
| PRJNA1139707 | ENA
Project description:To investigate the pathological effect of miR-126 on the progression of acute myeloid leukemia (AML) induced by AML1-ETO9a (AE9a), we conducted a series of mouse bone marrow transplantation (BMT) assays with the following groups: AE9a (primary donor cells were wild-type mouse bone marrow progenitor (i.e., lineage negative; Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), AE9a+miR-126 (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a-miR-126), and miR-126KO+AE9a (primary donor cells were miR-126 knockout mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), along with a control group (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG empty vector). The control group was only used in the primary and secondary BMT assays, whereas the three leukemic groups including AE9a, AE9a+miR-126 and miR-126KO+AE9a were used in four passages (i.e., primary, secondary, tertiary and quaternary) of BMT assays. Then, gene expression profiling was conducted with bone marrow samples collected from different groups to decipher the molecular mechanisms underlying miR-126 effects on leukemia initiation and progression and maintenance and self-renewal of leukemia stem/initiating cells. A total of 39 mouse bone marrow samples including 36 mouse AML samples with AE9a, AE9a+miR-126, and miR-126KO+AE9a collected from the 1st, 2nd, 3rd and 4th passages of BMT recipient mice (3 mice for each group in each passage), along with 3 normal controls from the 1st passage of BMT, were analyzed by use of Affymetrix GeneChip Mouse Gene 2.0 ST Array (Affymetirx, Santa Clara, CA). For each sample, the CD45.1+ cells (i.e., transplanted donor cells) were sorted with flow cytometry from whole BM cells collected from BMT recipient mice at the end stage. Then total RNA was isolated by use of miRNeasy extraction kit (Qiagen, Valencia, CA).
2015-09-07 | E-GEOD-65939 | biostudies-arrayexpress
Project description:To investigate the pathological effect of miR-126 on the progression of acute myeloid leukemia (AML) induced by AML1-ETO9a (AE9a), we conducted a series of mouse bone marrow transplantation (BMT) assays with the following groups: AE9a (primary donor cells were wild-type mouse bone marrow progenitor (i.e., lineage negative; Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), AE9a+miR-126 (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a-miR-126), and miR-126KO+AE9a (primary donor cells were miR-126 knockout mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), along with a control group (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG empty vector). The control group was only used in the primary and secondary BMT assays, whereas the three leukemic groups including AE9a, AE9a+miR-126 and miR-126KO+AE9a were used in four passages (i.e., primary, secondary, tertiary and quaternary) of BMT assays. Then, gene expression profiling was conducted with bone marrow samples collected from different groups to decipher the molecular mechanisms underlying miR-126 effects on leukemia initiation and progression and maintenance and self-renewal of leukemia stem/initiating cells.
2015-09-07 | GSE65939 | GEO