Transient Dicer deletion in ESCs
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE93725 | GEO | 2017/01/18
SECONDARY ACCESSION(S): PRJNA362205
REPOSITORIES: GEO
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Project description:To determine the spectrum of miRNA targets regulated following Dicer deletion, we performed argonaute 2 (AGO2)-RNA Immunoprecipitation (RIP)-microarray in bone marrow-derived macrophages (BMDMs) from LysM-Cre/Dicerflox/flox/Apoe–/– and LysM-Cre/Dicerwt/wt/Apoe–/– mice. This analysis combined with miRNA profiling in Dicer wild type (WT) and knockout (KO) BMDMs may help to identify the miRNA targets regulated by Dicer deletion.
2018-05-23 | GSE87717 | GEO
Project description:We have shown that Chrnb4-cre; Dicerflox/flox retinas (Dicer CKO) display a cone dystrophy by postnatal day P21, independent of rod degeneration. To elucidate which gene pathways were affected by Dicer loss, RNA sequencing was performed in whole neural retinas of P21 control and Dicer CKO mice. This experiment aims to identify which genes were differentially expressed between Dicer conditional knockout and control mice.
2019-01-14 | E-MTAB-6133 | biostudies-arrayexpress
Project description:We have shown that Chrnb4-cre; Dicerflox/flox retinas (Dicer CKO) display a cone dystrophy by postnatal day P21, independent of rod degeneration. To elucidate which miRNAs were involved in such phenotype, miRNA sequencing was performed in whole retinas of P21 and 3.5 month old control and Dicer CKO mice. This experiment aims to identify which miRNAs were differentially expressed in Dicer conditional knockout mice when compared to control mice.
2019-01-14 | E-MTAB-6132 | biostudies-arrayexpress
Project description:The endoribonuclease, Dicer, is indispensible for generating the majority of mature microRNAs (miRNAs), which are posttranscriptional regulators of gene expression involved in a wide range of developmental and pathological processes in mammalian central nervous system. While functions of Dicer-dependent miRNA pathways in neurons and oligodendrocytes have been extensively investigated, little is known about the role of Dicer in astrocytes. Here we report the effect of Cre-loxP mediated conditional deletion of Dicer selectively from postnatal astroglia on brain development. Dicer-deficient mice exhibited normal motor development and neurological morphology prior to postnatal week 5. Thereafter mutant mice invariably developed a rapidly fulminant neurological decline characterized by ataxia, severe progressive cerebellar degeneration, seizures, uncontrollable movements and premature death by postnatal week 9-10. Integrated transcription profiling, histological and functional analyses of cerebella showed that deletion of Dicer in cerebellar astrocytes altered the transcriptome of astrocytes to be more similar to an immature or reactive-like state prior to the onset of neurological symptoms or morphological changes. As a result, critical and mature astrocytic functions including glutamate uptake and antioxidant pathways were substantially impaired, leading to massive apoptosis of cerebellar granule cells and degeneration of Purkinje cells. Collectively, our study demonstrates the critical involvement of Dicer in normal astrocyte maturation and maintenance. Our findings also reveal non-cell autonomous roles of astrocytic Dicer-dependent pathways in regulating proper neuronal functions and implicate that loss of or dysregulation of astrocytic Dicer-dependent pathways may be involved in neurodegeneration and other neurological disorders. Four replicate experiments using samples derived from biologically independent pairs of control (mGfap-Cre; Dicer +/flox) and Dicer mutant (mGfap-Cre; Dicer flox/flox) littermate mice (postnatal day 30) were performed with a dye-swap experimental design.
2011-05-10 | E-GEOD-28589 | biostudies-arrayexpress
Project description:The global change of the miRNA expression profile during atherosclerosis is due to the infiltration of different types of leukocytes into the arterial vessel wall in addition to disease-specific regulation in vascular cells. Monocyte-derived macrophage accumulation in the subintimal region is critical in the formation of atherosclerotic plaques. However, the role of Dicer, the key enzyme for miRNA biogenesis, during the development of atherosclerosis is currently unknown. To detect the effect of Dicer on miRNA expression in macrophages, the comparison of the miRNA expression profiles was performed in bone marrow-derived macrophages (BMDMs) from LysM-Cre/Dicerflox/flox/Apoe–/– and LysM-Cre/Dicerwt/wt/Apoe–/– mice. This screening combined with miRNA profiling in atherosclerotic aortas may help to identify the crucial miRNAs that play a role in the macrophage function during atherogenesis.
2018-05-23 | GSE87718 | GEO
Project description:Increased monocyte adhesion to dysfunctional endothelial cells (ECs) orchestrated by chemokines plays an important role in arterial inflammation during atherosclerosis. Endothelial microRNAs (miRNAs) processed by the RNase Dicer1 determine the phenotype of ECs by posttranscriptional regulation of gene expression. However, the impact of endothelial miRNAs on endothelial inflammation and atherosclerosis is currently unclear. To study the effect of Dicer-dependent miRNAs in ECs on atherosclerosis, Apoe-/- mice with an inducible, EC-specific knock-out of Dicer (EC-Dicerflox) and control mice (EC-DicerWT) mice were treated with tamoxifen to induce Cre-recombinase activity and fed with a high fat-diet (HFD) for 12 weeks. The comparison of the miRNA expression profile in the aortas of EC-Dicerflox and EC-DicerWT mice after 12 weeks of a HFD was performed to identify EC-specific miRNAs that may play a role in the EC function during atherogenesis.
2015-05-31 | GSE53433 | GEO
Project description:Increased monocyte adhesion to dysfunctional endothelial cells (ECs) orchestrated by chemokines plays an important role in arterial inflammation during atherosclerosis. Endothelial microRNAs (miRNAs) processed by the RNase Dicer1 determine the phenotype of ECs by posttranscriptional regulation of gene expression. However, the impact of endothelial miRNAs on endothelial inflammation and atherosclerosis is currently unclear. To study the effect of Dicer-dependent miRNAs in ECs during the development of atherosclerosis, Apoe-/- mice with an inducible, EC-specific knock-out of Dicer (EC-Dicerflox) and control mice (EC-DicerWT) mice were treated with tamoxifen to induce Cre-recombinase activity and fed with a high fat-diet (HFD) for 4 weeks. The comparison of the miRNA expression profile in the aortas of EC-Dicerflox and EC-DicerWT mice after 4 weeks of a HFD was performed to identify EC-specific miRNAs that may play a role in the EC function during atherogenesis.
2015-05-31 | GSE53435 | GEO
Project description:Dicer is required for miRNA processing and RNA interference. Here we knocked out Dicer in SV40 T antigen immortalized subcutaneous preadipocytes isolated from Dicer flox mice by transducing these cells with adenoviruses harboring Cre recombinase. Control cells were transduced with adenovirus harboring GFP. We used microarrays to detail the gene expression profile of Dicer knockout preadipocytes.
2012-03-31 | GSE24683 | GEO
Project description:Dicer is required for miRNA processing and RNA interference. Here we knocked out Dicer in SV40 T antigen immortalized subcutaneous preadipocytes isolated from Dicer flox mice by transducing these cells with adenoviruses harboring Cre recombinase. Control cells were transduced with adenovirus harboring GFP. We used microarrays to detail the gene expression profile of Dicer knockout preadipocytes. Four days after adenovirus infection, cells were harvested for RNA isolation and hybridization on Affymetrix microarrays. At this point, Dicer knockout was confirmed by several methods.
2012-03-30 | E-GEOD-24683 | biostudies-arrayexpress
Project description:The endoribonuclease, Dicer, is indispensible for generating the majority of mature microRNAs (miRNAs), which are posttranscriptional regulators of gene expression involved in a wide range of developmental and pathological processes in mammalian central nervous system. While functions of Dicer-dependent miRNA pathways in neurons and oligodendrocytes have been extensively investigated, little is known about the role of Dicer in astrocytes. Here we report the effect of Cre-loxP mediated conditional deletion of Dicer selectively from postnatal astroglia on brain development. Dicer-deficient mice exhibited normal motor development and neurological morphology prior to postnatal week 5. Thereafter mutant mice invariably developed a rapidly fulminant neurological decline characterized by ataxia, severe progressive cerebellar degeneration, seizures, uncontrollable movements and premature death by postnatal week 9-10. Integrated transcription profiling, histological and functional analyses of cerebella showed that deletion of Dicer in cerebellar astrocytes altered the transcriptome of astrocytes to be more similar to an immature or reactive-like state prior to the onset of neurological symptoms or morphological changes. As a result, critical and mature astrocytic functions including glutamate uptake and antioxidant pathways were substantially impaired, leading to massive apoptosis of cerebellar granule cells and degeneration of Purkinje cells. Collectively, our study demonstrates the critical involvement of Dicer in normal astrocyte maturation and maintenance. Our findings also reveal non-cell autonomous roles of astrocytic Dicer-dependent pathways in regulating proper neuronal functions and implicate that loss of or dysregulation of astrocytic Dicer-dependent pathways may be involved in neurodegeneration and other neurological disorders.
2011-05-10 | GSE28589 | GEO