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MiRNA expression in the spleen of C57BL mice, p53-knockout C57BL mice, and NO2-knockout C57BL mice.

ABSTRACT: The goal of the study is to assess whether inflammation-induced oxidative and nitrosative stress modulates miRNA expression in mouse model deficient in either p53 or NOS2 RNA was extracted from the spleen of C57BL mice (WT, NOS2 knockout, and p53 knockout) that were C. Parvum treated or saline control treated. 4 or 5 mice were utilized for each grouping.

ORGANISM(S): Mus musculus

SUBMITTER: Ewy Mathe

PROVIDER: E-GEOD-30218 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Inflammation regulates microRNA expression in cooperation with p53 and nitric oxide.

Mathé Ewy E Nguyen Giang H GH Funamizu Naotake N He Peijun P Moake Matthew M Croce Carlo M CM Hussain S Perwez SP

International journal of cancer 20111101 3

microRNA (miRNA) are small non-coding RNA targeting mRNAs leading to their instability and diminished translation. Altered expression of miRNA is associated with cancer. Inflammation and nitric oxide modulates the development of lymphomas in p53 knockout mice and there exists a negative feedback loop between p53 and NOS2. Using a genetic strategy, we tested the hypothesis that inflammation-induced oxidative and nitrosative stress modulates miRNA expression in mouse model deficient in either p53 ...[more]

PMID: 22042537

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miRNA expression in the spleen of C57BL mice, p53-knockout C57BL mice, and NO2-knockout C57BL mice.

Project description:The goal of the study is to assess whether inflammation-induced oxidative and nitrosative stress modulates miRNA expression in mouse model deficient in either p53 or NOS2

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CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice.

Project description:Multiple sclerosis (MS) is an inflammatory disease in which myelin in the spinal cord is damaged. C-C chemokine receptor type 5 (CCR5) is implicated in immune cell migration and cytokine release in central nervous system (CNS). We investigated whether CCR5 plays a role in MS progression using a murine model, experimental autoimmune encephalomyelitis (EAE), in CCR5 deficient (CCR5-/-) mice. CCR5-/- and CCR5+/+ (wild-type) mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG35-55) followed by pertussis toxin, after which EAE paralysis was scored for 28 days. We found that clinical scoring and EAE neuropathology were lower in CCR5-/- mice than CCR5+/+ mice. Immune cells (CD3+, CD4+, CD8+, B cell, NK cell and macrophages) infiltration and astrocytes/microglial activation were attenuated in CCR5-/- mice. Moreover, levels of IL-1?, TNF-?, IFN-? and MCP-1 cytokine levels were decreased in CCR5-/- mice spinal cord. Myelin basic protein (MBP) and CNPase were increased while NG2 and O4 were decreased in CCR5-/- mice, indicating that demyelination was suppressed by CCR5 gene deletion. These findings suggest that CCR5 is likely participating in demyelination in the spinal cord the MS development, and that it could serve as an effective therapeutic target for the treatment of MS.

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ChIPseq of enterocytes of the jejunum from transgene C57BL/6 mice harboring a CKIαΔgut knock-out

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2020-02-25 | E-MTAB-7858 | biostudies-arrayexpress

Expression profiling analysis of mouse P4 cerebellum in CitK mutant mice proficient or knockout for P53

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2017-02-09 | GSE83465 | GEO

RNA-seq of bone marrow neutrophils from wild-type mice (C57BL/6) and CD40LG knockout mice.

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2021-08-07 | E-MTAB-10732 | biostudies-arrayexpress

Gene expression data from transgenic and knockout mice

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