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Myeloid cell derived inducible nitric oxide synthase suppresses M1 macrophage polarization

ABSTRACT: Analysis of gene expression between WT and iNOS defecient M1 macrophage

ORGANISM(S): Mus musculus

PROVIDER: GSE65436 | GEO | 2015/02/02

SECONDARY ACCESSION(S): PRJNA273989

REPOSITORIES: GEO

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Myeloid cell derived inducible nitric oxide synthase suppresses M1 macrophage polarization

Project description:Analysis of gene expression between WT and iNOS defecient M1 macrophage RNA microarray was performed using RNA isolated from M1 polarized macrophages from WT and iNOS deficient mice stimulated with LPS/IFNγ for 6 hours. Total RNA was extracted using a RNeasy plus kit (QIAGEN, Valencia, CA), and the array was performed on an Illumina MouseRef-8 v2.0 expression beadchip (Illumina, USA) by the Genomics Core Facility at the Mount Sinai School of Medicine.

2015-02-02 | E-GEOD-65436 | biostudies-arrayexpress

Myeloid cell-derived inducible nitric oxide synthase suppresses M1 macrophage polarization.

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Inducible nitric oxide synthase regulates macrophage polarization via the MAPK signals in concanavalin A-induced hepatitis.

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Melatonin suppresses macrophage cyclooxygenase-2 and inducible nitric oxide synthase expression by inhibiting p52 acetylation and binding.

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Hypothalamic Macrophage Inducible Nitric Oxide Synthase Mediates Obesity-Associated Hypothalamic Inflammation.

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Macrophage inducible nitric oxide synthase circulates inflammation and promotes lung carcinogenesis.

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Protein Modifications Driven by Nitric Oxide and Nitroxyl during Macrophage Proinflammatory Activation

Project description:Proinlfammatory stimulation of murine macrophages elicits profound metabolic changes. iNOS-derived Nitric oxide (NO) is both necessary and sufficient for the repression of OXPHOS and major mitochondrial rewiring of carbon fluxes during M1 polarization. Since inflammation results in broad proteomics changes with oxidative modifications of specific targets, we aim to understand how this is managed in absence of this important endogenous gas and its derived reductive nitrogen species like nitroxyl (HNO). We used proteomics to detail the mitochondrial proteome expression and status of cysteine modifications underlying proinflammatory stimulation and identified distinct targets of reversible and irreversible cysteine oxidations during this process in presence and absence of NOS2, RNS donors, and in exacerbating conditions of oxidative stress.

2023-07-03 | MSV000092336 | MassIVE

Redox couples of inducible nitric oxide synthase.

Project description: Not available

| S-EPMC2552398 | biostudies-literature

Nitric oxide in liver fibrosis: The role of inducible nitric oxide synthase.

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RNA editing enzyme APOBEC3A promotes pro-inflammatory (M1) macrophage polarization

Project description:Macrophages acquire a pro-inflammatory M1 phenotype in response to microbial products or pro-inflammatory cytokines through incompletely understood molecular mechanisms. We recently described the induction of APOBEC3A-mediated cellular site-specific cytosine-to-uracil (C>U) RNA editing during M1 macrophage polarization. However, the functional significance of this RNA editing is unknown. Here, we find that cellular RNA editing by APOBEC3A can also be induced by influenza or Maraba virus infections in normal macrophages, and by interferons in tumor-associated macrophages. Gene knockdown and RNA Seq analyses show that APOBEC3A induces C>U RNA editing (range 7%-88%) of 209 exonic or UTR sites in 203 genes during M1 polarization of monocyte-derived macrophages. The highest level of deleterious protein-recoding C>U RNA editing is observed in THOC5, which encodes a key nuclear protein implicated in the export of mRNAs during M-CSF driven macrophage differentiation. Knockdown of APOBEC3A in M1 macrophages reduces pro-inflammatory IL6, IL23A, and IL12B gene expression, CD80 and CD86 surface protein expression, and TNF-α, IL-1β and IL-6 cytokine secretion, and increases glycolysis and glycolytic capacity. These results demonstrate that APOBEC3A cytidine deaminase plays an important role in transcriptomic and functional polarization of pro-inflammatory M1 macrophages.

2020-03-13 | GSE146867 | GEO

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