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).
Project description:miR-127 is an imprinted microRNA on mouse chromosome 12, strongly expressed during late embryogenesis and known regulator of placental gene Rtl1. miR-127-knockout (KO) mice appear phenotypically normal. An Illumina beadchip whole genome microarray experiment was carried out on embryonic stage 18.5 (E18.5) mice with a deletion in the miR-127 gene, and compared with wild type (WT) mice. Three tissues with varying expression of miR-127 were analysed: brain, skin and muscle.
Project description:Recent genetic evidence has revealed microRNA-137 (miR-137) as a risk gene in schizophrenia and autism spectrum disorder (ASD), and the following cellular studies have demonstrated the importance of miR-137 in regulating neurogenesis. We have generated miR-137 knockout mice which display behaviors that resemble some symptoms of these two diseases. To investigate the underlying molecular mechanism, we performed comprehensive analyses of the entire RNA and protein molecules of the miR-137 mouse brains. The dataset uploaded here is the raw data of the mass spectrometry-based whole proteome analysis of the six miR-137 mouse brains: wild-type, heterozygous (miR-137+/–) and homozygous (miR-137–/–) from two different litters. The tandem mass tag (TMT) methodology was employed in this proteomics analysis for the quantitation. The sample channels are: 128C (miR-137+/+, litter 1), 129N (miR-137+/–, litter 1), 129C (miR-137–/–, litter 1), 130N (miR-137+/+, litter 2), 130C (miR-137+/–, litter 2), and 131N (miR-137–/–, litter 2).
Project description:Gene expression profiling of HCCs developed in miR-122 knockout mice compared to age-matched wild type mice. The significance of our study is that miR-122 knockout mice spontaneously develop liver tumors and the gene expression profile demonstrated dysregulation of several pathways involved in liver disease and HCC.
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.
Project description:Gene expression in wild-type and p38a-knockout keratinocytes were compared. Keratinocytes were isolated from newborn mice, and left unirradiated (0 h) and irradiated (4 h) with ultraviolet-B (UVB). C57BL/6 wild-type mice, and keratinocyte-specific p38a-knockout mice on a C57BL/6 background were used for isolation of primary keratinocytes.
Project description:Gene expression in wild-type and p38a-knockout dendritic cells (DCs) were compared. Lymph node dendritic cells were isolated from mice, and left unstimulated and stimulated with Pam3CSK4, a toll-like receptor 2 agonist. C57BL/6 wild-type mice, and dendritic cell-specific p38a-knockout mice on a C57BL/6 background were used for isolation of primary DCs.
Project description:Transcriptional profiling of mouse E16 epidermis deficient of Sox4, Sox11, or both as compared to gender matched wild type littermate controls. Goal was to identify the genes differentially expresssed in the conditional knockout epidermis vs the wild-type control epidermis.