Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microglia-astrocyte crosstalk regulates synapse remodeling via Wnt signaling

ABSTRACT: Unilateral whisker lesioning at age P4 leads to removal of thalamocortical synapses in layer IV of the barrel cortex over the course of the next 6 days. Synapse removal is mediated by microglia and induced by CX3CL1-CX3CR1 signaling between neurons and microglia. Downstream of CX3CL1-CX3CR1 activation, microglia induce astrocyte morphological changes. To identify molecular crosstalk between astrocytes and microglia, we performed translating ribosome affinty purification followed by RNA sequencing (TRAP-Seq).

ORGANISM(S): Mus musculus

PROVIDER: GSE252628 | GEO | 2025/08/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Microglia-astrocyte crosstalk regulates synapse remodeling via Wnt signaling

Project description:Unilateral whisker lesioning at age P4 leads to removal of thalamocortical synapses in layer IV of the barrel cortex over the course of the next 6 days. Synapse removal is mediated by microglia and induced by CX3CL1-CX3CR1 signaling between neurons and microglia. Downstream of CX3CL1-CX3CR1 activation, microglia induce astrocyte morphological changes and activation of canonical Wnt signaling in astrocytes. To explore the spatial pattern of microglia Wnt ligand expression and astrocyte Wnt receptor expression in astrocytes, we analyzed coronal sections containing the barrel cortex from 4 wild-type mice and 4 CX3CL1 knockout mice at 24 hours after whisker lesioning by multiplexed error-robust fluorescent in situ hybridization (MERFISH).

2025-09-10 | GSE298314 | GEO

Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling

Project description:Single-cell (inDrops) analysis of primary somatosensory cortex after early postnatal unilateral whisker lesioning

2019-04-02 | GSE129150 | GEO

Microglia regulate basal cerebral blood flow and neurovascular coupling through ectonucleotidase CD39

Project description:Microglia tightly interact with brain capillaries and regulate blood brain barrel permeability in pathological conditions. However, it is still unknown whether and how microglia regulate CBF in homeostatic condition. Here we show microglia directly regulate cerebral blood flow (CBF) and neurovascular coupling. Conditional knockout of microglial CD39 resulted in CBF hyper perfusion, reduced ATP induced CBF increase, impaired neurovascular coupling by whisker stimulation and reduced whisker stimulation induced adenosine increase in barrel cortex. Out data suggest that microglia is an important player for CBF regulation.

2023-07-01 | GSE223314 | GEO

Chromatin remodeler Arid1a regulates subplate neuron identity and wiring of cortical connectivity

Project description:Loss-of-function mutations in chromatin remodeler gene ARID1A are a cause of Coffin-Siris syndrome, a developmental disorder characterized by dysgenesis of corpus callosum. Here, we characterize Arid1a function during cortical development and find unexpectedly selective roles for Arid1a in subplate neurons. Subplate neurons (SPNs), strategically positioned at the interface of cortical grey and white matter, orchestrate multiple developmental processes indispensable for neural circuit wiring. We find that pan-cortical deletion of Arid1a leads to extensive mistargeting of intracortical axons and agenesis of corpus callosum. Sparse Arid1a deletion, however, does not autonomously misroute callosal axons, implicating non-cell autonomous Arid1a functions in axon guidance. Supporting this possibility, the ascending axons of thalamocortical neurons, which are not autonomously affected by cortical Arid1a deletion, are also disrupted in their pathfinding into cortex and innervation of whisker barrels. Coincident with these miswiring phenotypes, which are reminiscent of subplate ablation, we unbiasedly find a selective loss of SPN gene expression following Arid1a deletion. In addition, multiple characteristics of SPNs crucial to their wiring functions, including subplate organization, subplate-thalamocortical axon co-fasciculation (“handshake”), and extracellular matrix, are severely disrupted. To empirically test Arid1a sufficiency in subplate, we generate a cortical plate deletion of Arid1a that spares SPNs. In this model, subplate Arid1a expression is sufficient for subplate-thalamocortical axon co-fasciculation and extracellular matrix assembly. Consistent with these wiring functions, subplate Arid1a sufficiently enables normal callosum formation, thalamocortical axon targeting, and whisker barrel development. Thus, Arid1a is a multifunctional regulator of subplate-dependent guidance mechanisms essential to cortical circuit wiring.

2021-05-06 | GSE163273 | GEO

Transcriptional Profile of Brain Endothelial Cells in Response to Perturbations of Glutamatergic Neural Acticity

Project description:Bulk RNA sequencing of Brain Endothelial Cells from brain regions that underwent 3 hours of DREADDs-mediated glutamatergic activation or silencing compared to respective littermate controls or volitional whisker-mediated barrel cortex activation compared to no whisker controls.

2020-08-24 | GSE156689 | GEO

CX3CR1-Fractalkine Dysregulation Affects Retinal GFAP Expression, Inflammatory Gene Induction, and LPS Response in a Mouse Model of Hypoxic Retinopathy

Project description:Diabetic retinopathy (DR) causes vision loss due to sustained inflammation and vascular dam-age. The vascular damage is characterized fibrinogen leakage, angiogenesis, and hypoxia exac-erbating retinal damage. Neuronal regulation of microglia via the CX3CL1 (FKN)-CX3CR1 pathway also play a significant role in retinal pathology; here defects in the FKN-CX3CR1 pathway exacerbate inflammation, vascular damage and vision impairment. However, the con-tribution of hypoxic astrocytes to the pathological process of DR is unclear.

2025-02-17 | GSE276207 | GEO

The CX3CL1-CX3CR1 chemokine axis can contribute to tumor immune evasion and blockade with a novel CX3CR1 monoclonal antibody enhances responses to anti-PD-1 immunotherapy [CT26]

Project description:To investigate the imunoresistance programs regulated by the CX3CL1-CX3CR1 axis, we treated CT26 mouse tumor cell line with CX3CL1, CX3CL1 + IFN-γ, IFN-γ, and no treatment

2023-09-01 | GSE215269 | GEO

Microglia modulate the cerebrovascular reactivity through ectonucleotidase CD39

Project description:Microglia and the border-associated macrophages contribute to the modulation of cerebral blood flow, but the mechanisms have remained uncertain. Here, we show that microglia regulate the cerebral blood flow baseline and the responses to whisker stimulation or intra-cisternal magna injection of adenosine triphosphate, but not intra-cisternal magna injection of adenosine in mice model. Notably, microglia repopulation corrects these cerebral blood flow anomalies. The microglial-dependent regulation of cerebral blood flow requires the adenosine triphosphate-sensing P2RY12 receptor and ectonucleotidase CD39 that initiates the dephosphorylation of extracellular adenosine triphosphate into adenosine in both male and female mice. Pharmacological inhibition or CX3CR1-CreER-mediated deletion of CD39 mimics the cerebral blood flow anomalies in microglia-deficient mice and reduces the upsurges of extracellular adenosine following whisker stimulation. Together, these results suggest that the microglial CD39-initiated breakdown of extracellular adenosine triphosphate co-transmitter is an important step in neurovascular coupling and the regulation of cerebrovascular reactivity.

2024-06-01 | GSE245107 | GEO

ADAM17 in glutamatergic presympathetic neurons enhance angiotensin II-induced disinhibition and sympatho-excitation through microglia and chemotactic pathway

Project description:Background: Neuron-expressing ADAM17 (a disintegrin and metalloprotease 17) has been shown to support sympatho-excitation and salt-sensitive hypertension. The aim of current work was to identify by what mechanism ADAM17 in glutamatergic neurons support activation of presympathetic neurons (PSN). Methods: Both acute Ang-II stimulation in the PVN (paraventricular nucleus) and DOCA (deoxycorticosterone acetate)-salt model were utilized for electrophysiological recording and blood pressure (BP) recording, in mice with ADAM17 selective knockout in glutamatergic neurons (A17G), and ADAM17 targeted knockout in certain glutamatergic PVN-RVLM (rostral ventrolateral medulla) projecting neurons (PSN-A17G). Results: Both Ang-II and DOCA-salt treatment markedly decreased GABAergic inhibitory tone in the PVN of WT (wild-type) mice. Post DOCA-salt treatment, microglia were activated in the PVN, with significantly more expression of CD68 and related cytokines. With 7-day of DOCA-salt treatment, before BP arrived its plateau, PVN microglia had already been activated, and they were spotted more closely to virus-labeled glutamatergic PSN. Moreover, the number of GABAergic presynaptic terminals, locating on the soma area of PSN, was markedly reduced. In both A17G and PSN-A17G, these DOCA-salt-associated changes were blunted. Further experiments revealed that Ang-II promotes neuron-mediated chemotaxis for microglia, and this effect in neurons involved ADAM17 and its downstream – CX3CL1/CX3CR1 chemotactic pathway. Pharmacologically blocking CX3CR, or inhibiting migration of microglia, confirmed the contribution of CX3CL1/CX3CR1 signaling pathway and microglial displacement to Ang-II-induced disinhibition and activation of PSN.

2025-09-28 | GSE279173 | GEO

Differential regulation by CX3CR1 ligands CX3CL1 and CCL26 on mouse bone marrow-derived macrophages

Project description:We studied the effect of ligation on chemokine receptor CX3CR1 in the mouse bone marrow-derived macrophages (BMDM). We compared transcriptional profiles of BMDM treated with CX3CL1 and those of CCL26 to test if these two CX3CR1 ligands regulate differently.

2023-01-29 | GSE166291 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data