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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: Not available

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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.

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

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

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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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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

Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish

Project description:Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration, demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair, chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study, we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response, disrupted neutrophil migration, delayed fibrin clearance, and ultimately impaired heart regeneration. Transcriptome-wide RNA-seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably, partial inhibition of the pro-inflammatory cytokine Tnf-α rescued heart regeneration in the nr4a1 mutants, highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury.

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

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Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish

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Pattern separation memory requires Cerebellin 4-Neogenin 1 signaling at dentate gyrus synapses

Project description:The ability to avoid confusion between similar episodic memories enables organismal survival and fitness. This evolutionarily conserved differentiation process of memories as distinct representations is known as pattern separation. A central role for the entorhinal cortex->dentate gyrus (EC->DG) circuit in pattern separation is well established, but the molecular mechanisms that enable this circuit to mediate pattern separation memory is not known. Here we show the involvement in murine pattern separation memory of a unique transsynaptic protein complex formed by Cerebellin-4, Neogenin-1, and neurexins that is known to be selectively required for long-term plasticity in the EC->DG circuit. In vivo deletion of either presynaptic Cerebellin-4 in the entorhinal cortex or of postsynaptic Neogenin-1 in the dentate gyrus impairs acquisition of pattern separation memory. Thus, we describe a specific memory function for a defined molecular complex at an identified synapse, providing direct support for the hypothesis that synaptic plasticity contributes to the encoding of memory.

2026-04-17 | GSE273494 | GEO

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