Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA123689 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE19354: Expression data for rno-miR-146a overexpressing cell line HSC-2 GSE19462: microRNA profiling in vitro activated primary hepatic stellate cells Refer to individual Series
2010-05-18 | E-GEOD-19463 | biostudies-arrayexpress
Project description:Aging is associated with significant changes in the hematopoietic system, including increased inflammation, impaired hematopoietic stem cell (HSC) function, and increased incidence of myeloid malignancy. Inflammation of aging (“inflammaging”) has been proposed as a driver of age-related changes in HSC function and myeloid malignancy, but mechanisms linking these phenomena remain poorly defined. Here, we identify loss of miR-146a as driving aging-associated inflammation in AML patients. miR-146a expression declined in old wild-type mice, and loss of miR-146a promoted premature HSC aging and inflammation in young miR-146a-null mice, preceding development of aging-associated myeloid malignancy. Using single-cell assays of HSC quiescence, stemness, differentiation potential, and epigenetic state to probe HSC function and population structure, we found that loss of miR-146a depleted a subpopulation of primitive, quiescent HSCs. DNA methylation and transcriptome profiling implicated NF-κB, IL6, and TNF as potential drivers of HSC dysfunction, activating an inflammatory signaling relay promoting IL6 and TNF secretion from mature miR-146a-/- myeloid and lymphoid cells. Reducing inflammation by targeting Il6 or Tnf was sufficient to restore single-cell measures of miR-146a-/- HSC function and subpopulation structure, and reduced the incidence of hematological malignancy in miR 146a-/- mice. miR-146a-/- HSCs exhibited enhanced sensitivity to IL6 stimulation, indicating that loss of miR-146a affects HSC function via both cell-extrinsic inflammatory signals and increased cell-intrinsic sensitivity to inflammation. Thus, loss of miR 146a regulates cell-extrinsic and -intrinsic mechanisms linking HSC inflammaging to the development of myeloid malignancy.
2020-05-14 | GSE148989 | GEO
Project description:Aging is associated with significant changes in the hematopoietic system, including increased inflammation, impaired hematopoietic stem cell (HSC) function, and increased incidence of myeloid malignancy. Inflammation of aging (“inflammaging”) has been proposed as a driver of age-related changes in HSC function and myeloid malignancy, but mechanisms linking these phenomena remain poorly defined. Here, we identify loss of miR-146a as driving aging-associated inflammation in AML patients. miR-146a expression declined in old wild-type mice, and loss of miR-146a promoted premature HSC aging and inflammation in young miR-146a-null mice, preceding development of aging-associated myeloid malignancy. Using single-cell assays of HSC quiescence, stemness, differentiation potential, and epigenetic state to probe HSC function and population structure, we found that loss of miR-146a depleted a subpopulation of primitive, quiescent HSCs. DNA methylation and transcriptome profiling implicated NF-κB, IL6, and TNF as potential drivers of HSC dysfunction, activating an inflammatory signaling relay promoting IL6 and TNF secretion from mature miR-146a-/- myeloid and lymphoid cells. Reducing inflammation by targeting Il6 or Tnf was sufficient to restore single-cell measures of miR-146a-/- HSC function and subpopulation structure, and reduced the incidence of hematological malignancy in miR 146a-/- mice. miR-146a-/- HSCs exhibited enhanced sensitivity to IL6 stimulation, indicating that loss of miR-146a affects HSC function via both cell-extrinsic inflammatory signals and increased cell-intrinsic sensitivity to inflammation. Thus, loss of miR 146a regulates cell-extrinsic and -intrinsic mechanisms linking HSC inflammaging to the development of myeloid malignancy.
2020-05-14 | GSE148988 | GEO
Project description:Expression data from oligodendroglial cell line
| PRJNA225019 | ENA
Project description:To identify pathways and processes driving the observed hematopoietic stem cell (HSC) aging-like phenotypes in miR-146a-/- vs. WT, we performed RNA-seq gene expression profiling of Lin- Sca-1+ c-Kit+ (LSK) cells isolated from miR-146a-/- or WT mouse bone marrow (BM). Differential expression analysis and EnrichmentMap network analysis identified cytokine signalling and immune pathways as potential drivers of aging-like alterations in miR-146a-/- HSC proliferation and differentiation.
2020-05-14 | GSE148990 | GEO
Project description:Expression data from Sar1 isoform overexpressing rat hepatoma cell lines
| PRJNA230575 | ENA
Project description:We established stable miR-146a-5p overexpression T24 cells, then performed transcriptome profiling of miR-146a-5p overexpressing cells compared to control T24 cells to detect the molecular mechanisms of the miR-146a-5p’s effect on bladder cancer cells.
2024-02-03 | GSE166139 | GEO
Project description:HSC-2 (hepatic stellate cells line from rat) were stably transfected with rno-miR-146a. Three different clones were selected (S1, S4, S5). We used Affymetrix rat genome RAT230 2.0 chip to monitor global transcriptome changes. Two passages of each sample were used. Control - HSC-2 and GFPscr.
2009-12-07 | E-GEOD-19354 | biostudies-arrayexpress
Project description:HSC-2 (hepatic stellate cells line from rat) were stably transfected with rno-miR-146a. Three different clones were selected (S1, S4, S5). We used Affymetrix rat genome RAT230 2.0 chip to monitor global transcriptome changes.
2009-12-08 | GSE19354 | GEO
Project description:In order to identify the targets of miR-193a-5p in osteosarcoma U2OS cell line, we used a lentivirus-mediated expression system to overexpressing miR-193a precusor, miR-193a-5p target sequence and non-target sequence, respectively, in osteosarcoma cell line U2OS. A tandem mass tag (TMT)-based quantitative proteomic strategy was employed to identify the global profile of miR-193a-5p-regulated proteins. order to identify the targets of miR-193a-5p, we used a lentivirus-mediated expression system to overexpressing miR-193a precusor, miR-193a-5p target sequence and non-target sequence, respectively, in osteosarcoma cell line U2OS. A tandem mass tag (TMT)-based quantitative proteomic strategy was employed to identify the global profile of miR-193a-5p-regulated proteins.
2021-09-08 | PXD013987 | Pride