Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cytokine Polarized Bone Marrow Neutrophils Drive Axon Regeneration

ABSTRACT: Cytokine Polarized Bone Marrow Neutrophils Drive Axon Regeneration

PROVIDER: PRJNA1026311 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26329400_1.fastq.gz	Fastqsanger.gz
	SRR26329400_2.fastq.gz	Fastqsanger.gz
	SRR26329401_1.fastq.gz	Fastqsanger.gz
	SRR26329401_2.fastq.gz	Fastqsanger.gz
	SRR26329402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 84

Similar Datasets

Cytokine Polarized Bone Marrow Neutrophils Drive Axon Regeneration

Project description:The adult central nervous system (CNS) has a limited capacity for self-repair. Severed CNS axons typically do not regrow. There is an unmet need for treatments specifically designed to enhance neuronal viability, facilitate CNS axon regeneration, and ultimately restore lost neurological functions to individuals with traumatic CNS injury, multiple sclerosis, and stroke, among other disorders. Here we demonstrate that both mouse and human bone marrow (BM) neutrophils upregulate markers of alternative activation, and acquire the ability to promote neurite outgrowth, following polarization with a combination of recombinant interleukin-4 (IL-4) and granulocyte-colony stimulating factor (G-CSF). Moreover, adoptively transferring IL-4/G-CSF polarized BM neutrophils into experimental models of CNS injury resulted in significant axon regeneration within the optic nerve and spinal cord. The findings reported in this paper hold significant implications for the future development of autologous myeloid cell-based therapies that may bring us closer to effective solutions for reversing CNS damage.

2023-12-01 | GSE244934 | GEO

Polarized Dock Activity Drives Shh-Mediated Axon Guidance

Project description:Polarized Dock Activity Drives Shh-Mediated Axon Guidance

| PRJNA1118019 | ENA

Polarized Dock Activity Drives Shh-Mediated Axon Guidance

Project description:In the developing spinal cord, Sonic hedgehog (Shh) attracts commissural axons toward the floor plate. How Shh regulates the cytoskeletal remodeling that underlies growth cone turning is unknown. We found that Shh-mediated growth cone turning requires the activity of Docks, which are unconventional GEFs. Knockdown of Dock3 and 4, or their binding partner ELMO1 and 2, abolished commissural axon attraction by Shh in vitro. Dock3/4 and ELMO1/2 were also required for correct commissural axon guidance in vivo. Polarized Dock activity was sufficient to induce axon turning, indicating that Docks are instructive for axon guidance. Mechanistically, we show that Dock and ELMO interact with Boc, the Shh receptor, and that this interaction is reduced upon Shh stimulation. Furthermore, Shh stimulation translocates ELMO to the growth cone periphery and activates Rac1. This identifies Dock/ELMO as an effector complex of non-canonical Shh signaling and demonstrates the instructive role of GEFs in axon guidance.

2024-05-31 | GSE268644 | GEO

Neutrophils drive skin autoinflammation by releasing IL-26

Project description:Neutrophils drive skin autoinflammation by releasing IL-26

| PRJNA1074260 | ENA

Sphingolipid-dependent Dscam sorting regulates axon segregation

Project description:Neurons are highly polarized cells with distinct protein compositions in axonal and dendritic compartments. Cellular mechanisms controlling polarized protein sorting have been described for mature nervous system but little is known about the segregation in newly differentiated neurons. In a forward genetic screen for regulators of Drosophila brain circuit development, we identified mutations in <span style="color: rgb(54, 54, 54); font-style: normal; font-weight: 400; background-color: rgb(245, 245, 245);">Serine Palmitoyltransferase </span>(SPT), an evolutionary conserved enzyme in sphingolipid biosynthesis. Here we show that reduced levels of sphingolipids in SPT mutants cause axonal morphology defects similar to loss of cell recognition molecule Dscam. Loss- and gain-of-function studies show that neuronal sphingolipids are critical to prevent aggregation of axonal and dendritic Dscam isoforms, thereby ensuring precise Dscam localization to support axon branch segregation. Furthermore, SPT mutations causing neurodegenerative HSAN-I disorder in humans also result in formation of stable Dscam aggregates and axonal branch phenotypes in Drosophila neurons, indicating a causal link between developmental protein sorting defects and neuronal dysfunction.

2019-03-29 | MTBLS825 | MetaboLights

Runx1 negatively regulates inflammatory cytokine production by neutrophils in response to Toll-like receptor signaling: HP scRNA-seq

Project description:RUNX1 is frequently mutated in myeloid and lymphoid malignancies. It has been shown to negatively regulate Toll-like receptor 4 (TLR4) signaling through nuclear factor kappa-B (NF-κB) in lung epithelial cells. Here we show that RUNX1 regulates TLR1/2 and TLR4 signaling and inflammatory cytokine production by neutrophils. Hematopoietic-specific RUNX1 loss increased the production of pro-inflammatory mediators, including tumor necrosis factor α (TNF-α), by bone marrow (BM) neutrophils in response to TLR1/2 and TLR4 agonists. Hematopoietic RUNX1 loss also resulted in profound damage to the lung parenchyma following inhalation of the TLR4 ligand lipopolysaccharide (LPS). However, neutrophils with neutrophil-specific RUNX1 loss lacked the inflammatory phenotype caused by pan-hematopoietic RUNX1 loss, indicating that dysregulated TLR4 signaling is not due to loss of RUNX1 in neutrophils per se, and single cell RNA sequencing indicates the dysregulation originates in a neutrophil precursor. Enhanced inflammatory cytokine production by neutrophils following pan-hematopoietic RUNX1 loss correlated with increased degradation of the inhibitor of NF-κB signaling (IκBα), and RUNX1-deficient neutrophils displayed broad transcriptional upregulation of many of the core components of the TLR4 signaling pathway. Hence early, pan-hematopoietic RUNX1 loss de-represses an innate immune signaling transcriptional program that is maintained in terminally differentiated neutrophils, resulting in their hyper-inflammatory state. We hypothesize that inflammatory cytokine production by neutrophils may contribute to leukemia associated with inherited RUNX1 mutations.

2020-02-17 | GSE144482 | GEO

Runx1 negatively regulates inflammatory cytokine production by neutrophils in response to Toll-like receptor signaling: PMN bulk RNA-seq

2020-02-17 | GSE144481 | GEO

Polarized microtubule remodeling transforms the morphology of reactive microglia cells and drives cytokine release

Project description:Polarized microtubule remodeling transforms the morphology of reactive microglia cells and drives cytokine release

| PRJNA998376 | ENA

Resident Kupffer cells and neutrophils drive liver toxicity in cancer immunotherapy

Project description:Resident Kupffer cells and neutrophils drive liver toxicity in cancer immunotherapy

| PRJNA733462 | ENA

Resident Kupffer cells and neutrophils drive liver toxicity in cancer immunotherapy

Project description:Resident Kupffer cells and neutrophils drive liver toxicity in cancer immunotherapy

| PRJNA734933 | ENA