Inhibition of Neogenin Fosters Resolution of Inflammation and Tissue Regeneration
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA481264 | ENA |
REPOSITORIES: ENA
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Project description: Not available
| S-EPMC6159953 | biostudies-literature
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Project description:Alternatively activated macrophages (AAMs) contribute to the resolution of inflammation and tissue repair. However, molecular pathways that govern their differentiation upon tissue damage have remained incompletely understood. Here, we show that the transcription factor GATA3 specifically controls the IL-4-independent differentiation of pro-resolving and reparative AAMs in response to injury and the necrotic cell-derived alarmin IL-33. In macrophages, IL-33 sequentially triggered an early expression of pro-inflammatory genes as well as a subsequent differentiation into AAMs. Global analysis of involved signaling events identified an IL-33-induced GATA-3 transcriptional module that specifically orchestrated AAM differentiation. IL-4-induced AAM differentiation, in contrast, was independent of GATA-3. Conditional deletion of GATA-3 in mononuclear phagocytes accordingly abrogated IL-33-induced differentiation of AAMs in vitro and diminished macrophage-mediated tissue repair in vivo. Our data thus identify an IL-33-GATA3 signaling axis that controls plasticity of macrophages in response to injury and fosters resolution of inflammation.
2021-10-06 | GSE151654 | GEO
Project description:Alternatively activated macrophages (AAMs) contribute to the resolution of inflammation and tissue repair. However, molecular pathways that govern their differentiation upon tissue damage have remained incompletely understood. Here, we show that the transcription factor GATA3 specifically controls the IL-4-independent differentiation of pro-resolving and reparative AAMs in response to injury and the necrotic cell-derived alarmin IL-33. In macrophages, IL-33 sequentially triggered an early expression of pro-inflammatory genes as well as a subsequent differentiation into AAMs. Global analysis of involved signaling events identified an IL-33-induced GATA-3 transcriptional module that specifically orchestrated AAM differentiation. IL-4-induced AAM differentiation, in contrast, was independent of GATA-3. Conditional deletion of GATA-3 in mononuclear phagocytes accordingly abrogated IL-33-induced differentiation of AAMs in vitro and diminished macrophage-mediated tissue repair in vivo. Our data thus identify an IL-33-GATA3 signaling axis that controls plasticity of macrophages in response to injury and fosters resolution of inflammation.
2021-10-06 | GSE151653 | GEO
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Project description:In adult mammals, retinal ganglion cells (RGCs) fail to regenerate their axons when damaged. As a result, RGCs die after acute injury and in progressive degenerative diseases such as glaucoma; such damage can lead to permanent vision loss and blindness. Little is known about the roles of lipids in axon injury and repair despite their fundamental importance in composition of cell membranes, myelin sheaths and mediation of signaling pathways. Study of the lipidome in the biology of optic nerve (ON) regeneration has been largely neglected. A better understanding of the roles that lipids play in RGC biology may enhance understanding of RGC-related diseases and point to novel treatments. Established experimental models of ON regeneration allow exploration of molecular determinants of RGC axon regenerative success and failure. In this study, we used high-resolution liquid chromatography-tandem mass spectrometry to analyze lipidomic profiles of the ON and retina in an ON crush model with and without intravitreal Zymosan injections to enhance regeneration. Our results reveal profound remodeling of retina and ON lipidomes that occur after injury. In the retina, Zymosan treatment largely abrogates widespread lipidome alterations. In the ON, Zymosan induces lipid profiles that are distinct from those observed in naïve and vehicle-injected crush controls. We have identified a number of lipid species, classes and fatty acids that may be involved in the mechanisms of axon damage and repair. Lipids upregulated during RGC regeneration may be interesting candidates for further functional studies.
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Project description:The purpose of this study is to investigate how SREBP1a in macrophages regulates cellular function during muscle regeneration process after injury. We report that the systemic deletion of Srebf1, encoding SREBP1, and macrophage-specific deletion of Srebf1a, encoding SREBP1a, delays the resolution of inflammation, and impairs skeletal muscle regeneration after injury. Srebf1 deficiency impairs mitochondrial function of macrophages and suppresses the accumulation of reparative macrophages to the injured site.
2023-12-17 | GSE232394 | GEO
Project description:Mature myeloid cells play a crucial role in the pathogenesis of Crohn disease (CD) but the molecular players that regulate their functions in CD are not fully characterized. Here we show that Trim33 mRNA level is decreased in CD patient’s blood monocytes and characterize TRIM33 functions in monocytes during dextran sulfate sodium (DSS) induced colitis. Mice deleted for trim33 only in mature myeloid cells (Trim33-/- mice) display an impaired resolution of colonic inflammation. This deficiency is associated with an increased number of blood and colon neutrophils and monocytes and a decreased number of colonic macrophages. In accordance, Trim33-/- monocytes are less competent that wild type monocytes for recruitment and differentiation into macrophages at the inflammatory site. Furthermore, during resolution of DSS-induced colitis, Trim33-/- colonic macrophages display an impaired M1/M2 switch and express a low level of membrane bound TNFα known to regulate resolution of inflammation. Altogether, these results show an important role of TRIM33 in monocytes/macrophages during the resolution of DSS-induced colonic inflammation and pinpoint TRIM33 as a novel Crohn disease biomarker and as a potential therapeutic target.
2019-07-26 | GSE124778 | GEO
Project description:During the resolution of inflammation macrophages engulf apoptotic polymorphonuclear cells (PMN) and can accumulate large numbers of their corpses. Here we report that resolution-phase-macrophages acquire the neutrophil-derived glycoprotein lactoferrin (Lf) in vivo and ex vivo and process it to short fragments. During the onset and resolving phases of inflammation in murine peritonitis and bovine mastitis Lf fragments of 15 and 17 kDa occurred in various body fluids, and the murine fragmentation and release were mediated by macrophages. The 17 kDa fragment contained two bioactive tripeptides, FKD and FKE that promoted human macrophage reprogramming to a pro-resolving phenotype. At low concentrations (1-10 M) this was reflected by inhibition of LPS-induced TNFand IL-6 secretion and increased IL-10 levels. Both peptides inhibited ERK and cJun activation following macrophage exposure to LPS. In addition, FKD, and to a lesser extent FKE, promoted neutrophil-mediated resolution at high concentrations (30-100 M) by enhancing the formation of cytokine-scavenging aggregated NETs at low cellular density. Thus, PMN lactoferrin is acquired, processed and
2018-03-20 | PXD009190 | Pride