Ontology highlight
ABSTRACT:
PROVIDER: PRJNA854590 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNAs are small non-coding RNA molecules that fine-tune diverse biological processes and are often found to be dysregulated in diseases, such as multiple sclerosis (MS). MS is an immune-mediated disease of the central nervous system characterized by demyelination, axonal loss and neurodegeneration. We have previously shown microRNA-150 (miR-150) levels to be elevated in cell-free cerebrospinal fluid (CSF) of MS patients compared to controls. We aimed to investigate the physiopathological function of miR-150 in vivo by generating miR-150 knock-out (KO) and knock-in (KI) mice using CRISPR/Cas9 technology. To specifically interrogate the role of miR-150 upon inflammation of the central nervous system (CNS), we induced experimental autoimmune encephalomyelitis (EAE), a mouse model for MS, in these newly generated mice. After induction of EAE, miR-150KO mice developed milder disease compared to WT littermate controls while miR-150KI mice presented with exacerbated EAE. Disease amelioration in miR-150KO was accompanied by decreased infiltration of CD4+ T cells in the central nervous system compared to WT and KI mice, as well as increased FoxP3+ regulatory T (Treg) cells in inguinal lymph nodes at disease priming stage. We demonstrated that Treg cells were fundamental for EAE amelioration in miR-150KO mice, as their partial depletion during EAE priming stage in miR-150KO FoxP3DTR mice restored disease incidence and severity to the levels observed in WT and KI mice. Transcriptomic profiling of CD4+ T cells isolated from miR-150KO mice revealed upregulation of genes associated with Treg cell function, but also reduced gene translation and autophagy, as compared to WT and particularly KI cells. The role of miR-150 in affecting the fate of CD4+ T cells was further supported by the grater tendency of miR-150KO CD4+ T cells to differentiate into Treg cells in-vitro. In conclusion, miR-150 deficiency favored considerably milder CNS inflammation by promoting differentiation of a more anti-inflammatory CD4+ T cell repertoire.
2025-01-01 | GSE227844 | GEO
Project description:Small intestinal group 3 innate lymphoid cells (ILC3) from ILC3-conditional BMAL1 knock out mice or littermate control mice were sort-purified for transcriptional analysis
2019-08-28 | GSE135359 | GEO
Project description:MicroRNAs are small non-coding RNA molecules that have an important role in the fine tuning of all biological processes and are often found to be dysregulated in diseases, such as multiple sclerosis (MS). MS is an immune-mediated disease of the central nervous system characterized by demyelination, axonal loss and neurodegeneration. We have previously shown microRNA-150 (miR-150) levels to be elevated in cell-free cerebrospinal fluid (CSF) of MS patients compared to controls. The aim of this study is to further understand the physiopathological function of miR-150 using experimental autoimmune encephalomyelitis (EAE), a mouse model for MS. To establish its role in-vivo, we generated miR-150 knock-out (KO) and knock-in (KI) mice using CRISPR/Cas9. After induction of EAE, miR-150 KO mice showed ameliorated disease compared to WT littermate controls while miR-150 KI mice presented with exacerbated disease. An ameliorated disease in miR-150 KO was accompanied by a decreased infiltration of CD4 T cells compared to WT and KI. At priming stage of EAE we found that miR-150 KO had an increase in regulatory CD4 T cells (TREGS). Furthermore, after reconstitution of T cell deficient animals, CD4 T cells from miR-150 KO mice could protect against EAE and also showed an increased FOXP3 expression. A role of miR-150 in regulating TREG cells was further substantiated by transcriptome profiling, where miR-150 KO CD4 T cells suggested an enhancement of TREG phenotype as well as a diminished translation in miR-150 KO CD4 T cells. Moreover the results implicated miR-150 with mechanisms such as translation, autophagy and metabolism as well T cell proliferation and differentiation. In conclusion, miR-150 deficiency favored a more anti-inflammatory environment while miR-150 expression promoted pathogenic CD4 T cells subsets, potentially associated with metabolic mechanisms.
2025-01-01 | GSE167868 | GEO
Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we isolated small intestinal crypts and villus from wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (cKO) (Villin-Cre+; Lsd1f/f) mice. This experiment uses a new Cre strain with 100% recombination efficiency. RNA was directly isolated from the crypt and villus, and this was used for RNAseq. Gene expression analysis of cKO derived crypt and villus provides a spatially restricted outlook on the maturation status of the intestinal epithelium in the villi and the absence of Paneth cells in the crypt. Additionally, these mice were treated with antibiotics to study epithelium intrinsic changes related to LSD1 deletion but independent of the bacterial microbiome.
2023-08-02 | E-MTAB-10499 | biostudies-arrayexpress
Project description:The rs58542926 C>T variant of the transmembrane 6 superfamily member 2 gene (TM6SF2), encoding an E167K amino acid substitution, is associated with liver disease and cardiovascular disease. Therefore, we determined the long-term effects of this coding variant of TM6SF2 on glucose metabolism in mice with CRISPR/Cas9-mediated knock-in of TM6SF2 E167K (Tm6sf2 KI) and compared to littermate wild-type mice.
2021-10-15 | GSE146146 | GEO
Project description:We processed RNA-sequencing on splenic CD11b+ macrophages isolated from 10-week old Mettl3f/f-LysM-Cre KO and littermate WT mice. NO_4-1, NO_4-2 are Mettl3f/f-LysM-Cre KO. NO_5-2, NO_5-3 are WT littermate controls.
2022-01-07 | GSE184318 | GEO
Project description:Gene expression from 2 livers and 2 hearts from mouse Mut-ko/ki (MUT p.M700K) described in Forny et al JBC 2016 and 3 livers, 2 hearts from littermate controls
2019-09-22 | GSE121060 | GEO
Project description:Ribosome-bound mRNAs isolated from neurons in the hippocampi of Fmr1-/y mice and littermate WT controls
2022-06-07 | GSE199328 | GEO
Project description:Mucolipidosis type II (MLII) is a severe inherited multisystemic disorder caused by mutations in the GNPTAB gene. Skeletal abnormalities are a predominant feature of MLII. Here we investigate the gene expression in a knock-in mouse model for mucolipidosis type II, generated by the insertion of a cytosine in the murine Gnptab gene (c.3082insC) that is homologous to a homozygous mutation in an MLII patient. Since osteoblasts are critically involved in regulating bone development and remodeling, a genome-wide expression analysis was performed with RNA isolated from primary cultures of osteoblasts originating from MLII knock-in mice (KI) compared to RNA from wild-type (WT) osteoblasts to identify dysregulated genes involved in pathogenic mechanisms. Primary osteoblasts were isolated from calvaria of 5-day-old wild-type (WT) and MLII knock-in littermates (KI). RNA was extracted at day 10 of differentiation induced by ascorbic acid and beta-glycerophosphate and hybridization on Affymetrix microarrays. We used preparations of RNA from two individual primary cultures of osteoblasts for every genotype (WT_OB_I, WT_OB_II, KI_OB_I, KI_OB_II) and compared WT vs KI samples.
2014-01-29 | E-GEOD-43854 | biostudies-arrayexpress
Project description:IgA+ Plasma Cells were sort-purified from the small intestinal lamina prorpia of mice with a B cell lineage-intrinsic deletion of Arntl (Mb1 Cre+/- x Arntl fl/fl) or Cre negative littermate controls (also deisgnated WT and KO), at two Zeitgeber time points (ZT0 and ZT12). RNA extracted from these samples was subjected to bulk RNA seq to identify time of day differences and to compare role of Arntl expression in this context.
2022-09-02 | GSE175609 | GEO