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Inhibition of Neogenin Fosters Resolution of Inflammation and Tissue Regeneration

ABSTRACT: Inhibition of Neogenin Fosters Resolution of Inflammation and Tissue Regeneration

PROVIDER: PRJNA481264 | ENA |

REPOSITORIES: ENA

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Inhibition of neogenin fosters resolution of inflammation and tissue regeneration.

Project description:The resolution of inflammation is an active process that is coordinated by endogenous mediators. Previous studies have demonstrated the immunomodulatory properties of the axonal guidance proteins in the initial phase of acute inflammation. We hypothesized that the neuronal guidance protein neogenin (Neo1) modulates mechanisms of inflammation resolution. In murine peritonitis, Neo1 deficiency (Neo1-/-) resulted in higher efficacies in reducing neutrophil migration into injury sites, increasing neutrophil apoptosis, actuating PMN phagocytosis, and increasing the endogenous biosynthesis of specialized proresolving mediators, such as lipoxin A4, maresin-1, and protectin DX. Neo1 expression was limited to Neo1-expressing Ly6Chi monocytes, and Neo1 deficiency induced monocyte polarization toward an antiinflammatory and proresolving phenotype. Signaling network analysis revealed that Neo1-/- monocytes mediate their immunomodulatory effects specifically by activating the PI3K/AKT pathway and suppressing the TGF-β pathway. In a cohort of 59 critically ill, intensive care unit (ICU) pediatric patients, we found a strong correlation between Neo1 blood plasma levels and abdominal compartment syndrome, Pediatric Risk of Mortality III (PRISM-III) score, and ICU length of stay and mortality. Together, these findings identify a crucial role for Neo1 in regulating tissue regeneration and resolution of inflammation, and determined Neo1 to be a predictor of morbidity and mortality in critically ill children affected by clinical inflammation.

| S-EPMC6159953 | biostudies-literature

Inhibition of Neogenin Fosters Resolution of Inflammation and Tissue Regeneration

Project description:Protein and phosphorylation (TGF-β Phospho Antibody Array, FullMoonBioscience, #PTG176) profiling of peritoneal monocytes (pooled lavages from 4 mice / condition) was carried out according to the manufacturer’s instructions.

2018-07-18 | GSE117137 | GEO

Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination

Project description:Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination

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Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq II]

Project description:Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq II]

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Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq I]

Project description:Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq I]

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Inhibition of O-GlcNAcylation via O-GlcNAc transferase fosters megakaryopoiesis and induces thrombopoiesis

Project description:Inhibition of O-GlcNAcylation via O-GlcNAc transferase fosters megakaryopoiesis and induces thrombopoiesis

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IL-33-induced metabolic reprogramming controls the differentiation of alternatively activated macrophages and the resolution of inflammation (scRNA-seq)

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

IL-33-induced metabolic reprogramming controls the differentiation of alternatively activated macrophages and the resolution of inflammation (bulk RNA-seq)

2021-10-06 | GSE151653 | GEO

Inhibition of endothelial Notch signaling attenuates inflammation

Project description:Inhibition of endothelial Notch signaling attenuates inflammation

| PRJNA339936 | ENA

Lipidomics of inflammation-induced optic nerve regeneration

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.

2018-04-17 | ST000963 | MetabolomicsWorkbench

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