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Hif-1α stabilisation polarises macrophages via cyclooxygenase/prostaglandin E2 in vivo

https://doi.org/10.1101/536862
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Outgoing claims: the papers this work cites, builds on, or argues with.

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Interaction of Pattern Recognition Receptors with Mycobacterium Tuberculosis
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Tumor necrosis factor-α is required in the protective immune response against mycobacterium tuberculosis in mice
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Infectious Disease Modeling and Innate Immune Function in Zebrafish Embryos
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Transcriptomic Approaches in the Zebrafish Model for Tuberculosis—Insights Into Host- and Pathogen-specific Determinants of the Innate Immune Response
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An Integrated Model of Eicosanoid Metabolism and Signaling Based on Lipidomics Flux Analysis
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Stabilization of HIF-1α by FG-4592 promotes functional recovery and neural protection in experimental spinal cord injury
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The lta4h Locus Modulates Susceptibility to Mycobacterial Infection in Zebrafish and Humans
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Host Genotype-Specific Therapies Can Optimize the Inflammatory Response to Mycobacterial Infections
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The DNA Damage-Regulated Autophagy Modulator DRAM1 Links Mycobacterial Recognition via TLR-MYD88 to Autophagic Defense
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Live Imaging of Tumor Initiation in Zebrafish Larvae Reveals a Trophic Role for Leukocyte-Derived PGE2
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Targeting the 15-keto-PGE2-PTGR2 axis modulates systemic inflammation and survival in experimental sepsis
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Tumor Necrosis Factor Signaling Mediates Resistance to Mycobacteria by Inhibiting Bacterial Growth and Macrophage Death
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Macrophage Activation and Polarization: Nomenclature and Experimental Guidelines
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Risk of tuberculosis infection in anti-TNF-α biological therapy: From bench to bedside
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Specificity of the zebrafish host transcriptome response to acute and chronic mycobacterial infection and the role of innate and adaptive immune components
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Polarization of immune responses in fish: The ‘macrophages first’ point of view
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Prostaglandin catabolizing enzymes
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HIF-1α Is Essential for Myeloid Cell-Mediated Inflammation
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Tumour necrosis factor, interleukin-1 and adenosine deaminase in tuberculous pleural effusion
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Macrophages and control of granulomatous inflammation in tuberculosis
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Interception of host angiogenic signalling limits mycobacterial growth
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Mycobacterium tuberculosis suppresses innate immunity by coopting the host ubiquitin system
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Metabolism of PGE2 by prostaglandin dehydrogenase is essential for remodeling the ductus arteriosus
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Interdependence of hypoxic and innate immune responses
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Transcriptional landscape of Mycobacterium tuberculosis infection in macrophages
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COX2 is involved in hypoxia-induced TNF-α expression in osteoblast
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Cryptococcus neoformans Intracellular Proliferation and Capsule Size Determines Early Macrophage Control of Infection
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Macrophage arginase-1 controls bacterial growth and pathology in hypoxic tuberculosis granulomas
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Epigenetic control of intestinal barrier function and inflammation in zebrafish
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The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment
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Hypoxia activates the cyclooxygenase-2–prostaglandin E synthase axis
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Macrophage form, function, and phenotype in mycobacterial infection: lessons from tuberculosis and other diseases
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Zebrafish
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Macrophage defense mechanisms against intracellular bacteria
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Involvement of COX‐2/PGE2 signalling in hypoxia‐induced angiogenic response in endothelial cells
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Pharmacological Characterization of 1-(5-Chloro-6-(trifluoromethoxy)-1H-benzoimidazol-2-yl)-1H-pyrazole-4-carboxylic Acid (JNJ-42041935), a Potent and Selective Hypoxia-Inducible Factor Prolyl Hydroxylase Inhibitor
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Tuberculous Granulomas Are Hypoxic in Guinea Pigs, Rabbits, and Nonhuman Primates
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Tumor Necrosis Factor Alpha-Induced Hypoxia-Inducible Factor 1α–β-Catenin Axis Regulates Major Histocompatibility Complex Class I Gene Activation through Chromatin Remodeling
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Tuberculosis and anti-TNF- treatment
inferredcites →https://doi.org/10.1155/2013/683405openalex-snapshot
The Immunobiology of Prostanoid Receptor Signaling in Connecting Innate and Adaptive Immunity
inferredcites →https://doi.org/10.1155/2014/149185openalex-snapshot
Chronic Inflammation and Cytokines in the Tumor Microenvironment
inferredcites →https://doi.org/10.1158/0008-5472.can-06-0425openalex-snapshot
Direct Transcriptional Up-regulation of Cyclooxygenase-2 by Hypoxia-Inducible Factor (HIF)-1 Promotes Colorectal Tumor Cell Survival and Enhances HIF-1 Transcriptional Activity during Hypoxia
inferredcites →https://doi.org/10.1158/0008-5472.can-11-3148openalex-snapshot
A Zebrafish Model to Study and Therapeutically Manipulate Hypoxia Signaling in Tumorigenesis
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Abstract 4017: Gene silencing of EREG mediated by DNA methylation and histone modification in human gastric cancers
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The zebrafish lysozyme C promoter drives myeloid-specific expression in transgenic fish
inferredcites →https://doi.org/10.1189/jlb.0311153openalex-snapshot
Specificity of eicosanoid production depends on the TLR-4-stimulated macrophage phenotype
inferredcites →https://doi.org/10.1189/jlb.0409255openalex-snapshot
Pivotal Advance: Pharmacological manipulation of inflammation resolution during spontaneously resolving tissue neutrophilia in the zebrafish
inferredcites →https://doi.org/10.1189/jlb.1112594openalex-snapshot
Zebrafish as a model for the study of neutrophil biology
inferredcites →https://doi.org/10.1242/dmm.006676openalex-snapshot
Zebrafish embryo screen for mycobacterial genes involved in the initiation of granuloma formation reveals a newly identified ESX-1 component
inferredcites →https://doi.org/10.1242/dmm.021865openalex-snapshot
Exploring the HIFs, buts and maybes of hypoxia signalling in disease: lessons from zebrafish models
inferredcites →https://doi.org/10.1371/journal.pone.0100928openalex-snapshot
Mycobacteria Counteract a TLR-Mediated Nitrosative Defense Mechanism in a Zebrafish Infection Model
inferredcites →https://doi.org/10.1371/journal.pone.0129744openalex-snapshot
Mycobacterium tuberculosis-Induced Polarization of Human Macrophage Orchestrates the Formation and Development of Tuberculous Granulomas In Vitro
inferredcites →https://doi.org/10.1371/journal.ppat.1003789openalex-snapshot
Hypoxia Inducible Factor Signaling Modulates Susceptibility to Mycobacterial Infection via a Nitric Oxide Dependent Mechanism
inferredcites →https://doi.org/10.2217/fmb.15.11openalex-snapshot
Macrophage Takeover and the Host–bacilli interplay During Tuberculosis
inferredcites →https://doi.org/10.31768/2312-8852.2016.38(1):9-12openalex-snapshot
HIF-1 — A BIG CHAPTER IN THE CANCER TALE
inferredcites →https://doi.org/10.3389/fcimb.2012.00145openalex-snapshot
Mycobacterial signaling through toll-like receptors
inferredcites →https://doi.org/10.3389/fimmu.2014.00614openalex-snapshot
Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance
inferredcites →https://doi.org/10.3791/3781openalex-snapshot
Infection of Zebrafish Embryos with Intracellular Bacterial Pathogens
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Cutting Edge: Essential Role of Hypoxia Inducible Factor-1α in Development of Lipopolysaccharide-Induced Sepsis
inferredcites →https://doi.org/10.4049/jimmunol.181.6.3733openalex-snapshot
Macrophage Polarization in Bacterial Infections
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Identification of polarized macrophage subsets in zebrafish

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inferred← citeshttps://doi.org/10.3389/fimmu.2019.02321openalex-snapshot
Hypoxia Induces Macrophage tnfa Expression via Cyclooxygenase and Prostaglandin E2 in vivo
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