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Molecular and anatomical roadmap of stroke pathology in immunodeficient mice

ABSTRACT: Here, we assessed the stroke pathology of popular genetic immunodeficient mouse models using NOD scid gamma (NSG) and recombination activating gene 2 (Rag2–/–) mice as well as pharmacologically immunosuppressed mice and compared them to immune competent, wildtype (WT) C57BL/6J mice three weeks after injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE208605 | GEO | 2022/10/01

REPOSITORIES: GEO

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Gene expression profiles of MLL-AF9 leukemia cells in C57BL/6 mice and Rag2-/- mice

Project description:The relative importance of T/B lymphocytes and NK cells during acute myeloid leukemia (AML) progression has been unclear. In this study, we compared gene expression profiles of mouse AML cells expressing MLL-AF9 collected from immunologically normal wild-type (WT) C57BL/6 mice, Rag2-/- mice lacking mature T and B cells, and NSG mice lacking T, B and NK cells.

2023-12-27 | GSE245359 | GEO

The opposing impacts of dietary methionine restriction on tumor growth in immunodeficient and immunocompetent mice

Project description:Methionine, a sulfur-containing essential amino acid, is a key component of dietary proteins important for protein synthesis, sulfur metabolism, antioxidant defense, and signaling. However, the role of methionine in cancer progression remains inconclusive. On one hand, dietary methionine restriction is known to repress cancer growth and improve cancer therapy in xenografted tumors. On the other hand, methionine is also critical for T cell activation and differentiation, making it a potential tumor suppression nutrient by enhancing T cell-mediated anti-tumor immunity. Here we investigated the interaction between dietary methionine, immune cells, and cancer cells by allografting CT26.WT mouse colon carcinoma cells into immunocompetent Balb/c mice or immunodeficient NSG mice, then analyzed how dietary methionine contents affect their growth. Our results show that dietary methionine restriction suppresses tumor growth in immunodeficient NSG mice but promotes tumor progression in immunocompetentt Balb/c mice.

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BRAFV600E or mutant MAP2K1 human CD34+ cells establish Langerhans cell-like histiocytosis in immunodeficient mice

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Acute stroke imaging research roadmap.

Project description: Not available

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Hes6 expression is controlled by c-Myc and the AR to promote E2F1 activity and poor outcome in castrate-resistant prostate cancer (xenografts)

Project description:Hes6 is a transcription co-factor that is associated with stem cell characteristics in neural tissue, but its role in cancer remains uncertain. Here we show that Hes6 is controlled by c-Myc and the AR and can drive castration resistance in xenografts of the androgen-dependent LNCaP prostate cancer cell line model. Hes6 activates a cell cycle enhancing transcriptional network that maintains tumour growth in the absence of circulating androgen but with maintained nuclear AR. We demonstrate interaction between E2F1, the AR and Hes6 and show the co-dependency of these factors in the castration-resistant setting. In the clinical setting, we have discovered a Hes6-associated signature that predicts poor outcome in prostate cancer, which could be pharmacologically targeted. LNCaP-LM (luciferase expressing) cells with stable Hes6-overexpression and empty vector controls injected dorso-subcutaneously into NOD SCID gamma (NSG) mice. Mice were castrated when average graft size reached 100mm3 . Mice were culled after 12 weeks growth and grafts harvested.

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Proteomic analysis of bronchoalveolar lavage fluid during invasive pulmonary aspergillosis in mice and humans

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Transcriptomic analysis of femoral diaphysis and primary osteoprogenitor cells cultures from mouse strains with SHIP1 deficiency and controls

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Comparison of gene expression profile in RAG2+ B lineage cells from the small intestinal lamina propria and RAG2+ B lineage cells from the bone marrow

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Comparison of gene expression profile in RAG2+ B lineage cells from the small intestinal lamina propria and RAG2+ B lineage cells from the bone marrow

Project description:We used a RAG2-GFP reporter mouse to show that RAG+ B lineage cells can be found in the small intestinal lamina proria in normally-housed mice at weaning age. We used microarry expression analysis to compare the RAG2+ population in the gut to the RAG2+ B lineage population in the bone marrow. Microarray was used to compare RAG2+ lamina propria B cells to RAG2+ bone marrow B cells. For each experiment, RAG2-GFP+ cells from 8-12 post-natal day 17-25 RAG2-GFP reporter mice were sorted from small intestinal lamina propria lymphocyte preparations and bone marrow. RNA extracted from trizol was used for the analysis. 3 independent replicates were performed.

2013-07-12 | E-GEOD-48805 | biostudies-arrayexpress

Tau exacerbates excitotoxic brain damage in an animal model of stroke

Project description:Neuronal excitotoxicity induced by aberrant excitation of glutamatergic receptors contributes to brain damage in stroke. Here, we show that tau-deficient (tau-/-) mice are profoundly protected from excitotoxic brain damage and neurological deficits following experimental stroke, using a middle cerebral artery occlusion (MCAO) with reperfusion model. Mechanistically, we show that this protection is due to site-specific inhibition of glutamate-induced and Ras/ERK-mediated toxicity by accumulation of Ras-inhibiting SynGAP1, which resides in a post-synaptic complex with tau. Accordingly, reducing SynGAP1 levels in tau-/- mice abolished the protection from pharmacologically induced excitotoxicity and MCAO-induced brain damage. Conversely, over-expression of SynGAP1 prevented excitotoxic ERK activation in wild-type neurons. Our findings suggest that tau mediates excitotoxic Ras/ERK signaling by controlling post-synaptic compartmentalization of SynGAP1.

2017-09-01 | GSE45703 | GEO

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