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Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling

ABSTRACT: Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling

PROVIDER: PRJNA530236 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8833310.fastq.gz	Fastqsanger.gz
	SRR8833320.fastq.gz	Fastqsanger.gz
	SRR8833311.fastq.gz	Fastqsanger.gz
	SRR8833312.fastq.gz	Fastqsanger.gz
	SRR8833313.fastq.gz	Fastqsanger.gz

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Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling.

Project description:Microglia rapidly respond to changes in neural activity and inflammation to regulate synaptic connectivity. The extracellular signals, particularly neuron-derived molecules, that drive these microglial functions at synapses remain a key open question. Here we show that whisker lesioning, known to dampen cortical activity, induces microglia-mediated synapse elimination. This synapse elimination is dependent on signaling by CX3CR1, the receptor for microglial fractalkine (also known as CXCL1), but not complement receptor 3. Furthermore, mice deficient in CX3CL1 have profound defects in synapse elimination. Single-cell RNA sequencing revealed that Cx3cl1 is derived from cortical neurons, and ADAM10, a metalloprotease that cleaves CX3CL1 into a secreted form, is upregulated specifically in layer IV neurons and in microglia following whisker lesioning. Finally, inhibition of ADAM10 phenocopies Cx3cr1-/- and Cx3cl1-/- synapse elimination defects. Together, these results identify neuron-to-microglia signaling necessary for cortical synaptic remodeling and reveal that context-dependent immune mechanisms are utilized to remodel synapses in the mammalian brain.

| S-EPMC6596419 | biostudies-literature

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

Expression data from Adam10 knock out mice and wild type

Project description:Adam10, a cell surface protease, cleaving many proteins including TNF-alpha and E-cadherin. Here we investigate the genome wide effects of Adam10 knock out on the transcriptome. Commercial microarrays (Affymetrix Mouse Gene ST 1.0) were used to generate genome wide mRNA profiles. Mouse tissue samples from n=4 wiltype skin and n=4 Adam10 knockout skin were used in the study.

2011-01-06 | E-GEOD-25480 | biostudies-arrayexpress

Hypoxia dysregulates circadian rhythm and causes synapse elimination defects in astrocytes

Project description:Hypoxia dysregulates circadian rhythm and causes synapse elimination defects in astrocytes

| PRJNA1075676 | ENA

Human oligodendrocyte progenitor cells mediate synapse elimination through TAM receptor activation

Project description:Human oligodendrocyte progenitor cells mediate synapse elimination through TAM receptor activation

| PRJNA1013023 | ENA

Systematic substrate identification reveals a central role for the metalloprotease ADAM10 in axon targeting and synapse function

Project description:Metzincin metalloproteases have major roles in intercellular communication by modulating the function of membrane proteins. One of the proteases is the a-disintegrin-and-metalloprotease 10 (ADAM10) which acts as alpha-secretase of the Alzheimer’s disease amyloid precursor protein. ADAM10 is also required for neuronal network functions in murine brain, but neuronal ADAM10 substrates are only partly known. With a proteomic analysis of Adam10-deficient neurons we identified 91, mostly novel ADAM10 substrate candidates, making ADAM10 a major protease for membrane proteins in the nervous system. Several novel substrates, including the neuronal cell adhesion protein NrCAM, are involved in brain development. Indeed, we detected mistargeted axons in the olfactory bulb of conditional ADAM10-/- mice, which correlate with reduced cleavage of NrCAM, NCAM and other ADAM10 substrates. In summary, the novel ADAM10 substrates provide a potential molecular basis for neuronal network dysfunctions in conditional ADAM10-/- mice and demonstrate a fundamental function of ADAM10 as a sheddase in the brain.

2018-10-18 | PXD003426 | Pride

Adult cardiomyocytes treated with fractalkine (CX3CL1)

Project description:Background and Aims: It is known that inflammatory processes are activated in heart failure, but the regulation of cytokines and their role in the pathogenesis of the disease are not well understood. We have identified fractalkine as a possible novel mediator in HF development. To address this issue, we have performed microarray analysis of cardiomyocytes treated with different isoforms of fractalkine. Methods: Cardiomyocytes isolated from adult rat hearts and treated with different forms of fractalkine for 24 hours. Control cells were treated with BSA. Molecular alterations in myocardial tissue were measured by using cDNA microarrays. Molecular pathways affected were identified by the Ingenuity Pathway Analysis software. Results: Several molecular pathways were affected upon fractalkine stimulation of adult cardiomyocytes. Keywords: Fractalkines effect on cardiomyocytes

2008-02-01 | GSE7397 | GEO

Complement C1q-dependent synapse elimination by astrocytes in a mouse model of Alzheimer's disease

Project description:Synapse loss and glial activation are hallmarks of Alzheimer's disease (AD). In Tau P301S transgenic mice, the complement pathway contributes to neuronal damage through microglial elimination of synapses. Here, we used unbiased proteomic profiling of postsynaptic density (PSD) fractions from Tau P301S mice in C1q-WT versus C1q knockout backgrounds to identify C1q-dependent changes at synapses. Integrative multi-omics analysis revealed that astrocyte- and microglia- specific proteins are increased in Tau P301S synapse fractions with age and in a C1q-dependent manner. The same set of glial proteins (including C1q, C4, Gpnmb, and S100a4) is elevated in human AD synaptic fractions, and C4 levels are raised in cerebrospinal fluid (CSF) from AD patients. Besides microglia, we show that astrocytes contribute substantially to excitatory and inhibitory synapse engulfment in Tau P301S hippocampus. Based on staining of synapse markers within lysosomes, astrocytes showed preference for excitatory synapses whereas microglia preferred to engulf inhibitory synapse markers. Genetic deletion of C1q reduced astrocytic eating of excitatory and inhibitory synapses in Tau P301S mice, and rescued synapse density. Together, our data indicate that astrocytes contact and phagocytose synapses in a C1q- dependent manner and thereby contribute to synapse loss and neurodegeneration in AD.

2021-11-03 | MSV000088313 | MassIVE

The transcriptome of TRPV1-positive sensory neurons revealed by subgroup-elimination transcriptomics

Project description:The transcriptome of TRPV1-positive sensory neurons revealed by subgroup-elimination transcriptomics

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Transcription profiling of mouse adult cardiomyocytes treated with fractalkine (CX3CL1)

2008-06-18 | E-GEOD-7397 | biostudies-arrayexpress