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Myeloid C3 causes neuronal injury prior to synapse loss [snMulti-ome-seq]

ABSTRACT: Myeloid C3 causes neuronal injury prior to synapse loss [snMulti-ome-seq]

PROVIDER: PRJNA1084767 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR28242606_1.fastq.gz	Fastqsanger.gz
	SRR28242606_2.fastq.gz	Fastqsanger.gz
	SRR28242607_1.fastq.gz	Fastqsanger.gz
	SRR28242607_2.fastq.gz	Fastqsanger.gz

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Myeloid C3 causes neuronal injury prior to synapse loss [snMulti-ome-seq]

Project description:Complement component C3 mediates pathology in several CNS neurodegenerative diseases, but the cellular and molecular mechanisms leading to neuronal injury remain unclear. Herein, we examined how C3 deletion affects glial profiles and anterior visual pathway pathology in an animal model of neuroinflammation. scRNA-seq from mouse brain and optic nerve revealed that C3 expression defined disease-associated glial subtypes which were characterized by increased mTOR activation, cell metabolism, and translation. Deletion of C3 restored these glia towards homeostatic profiles. Myeloid-derived C3 mediated injury in optic nerve axons and retinal ganglion cells (RGCs) at the peak of EAE. To elucidate the timing of pathology we examined retinas prior to symptom onset and found reductions in Brn3a, an RGC transcription factor involved in dendritic arborization and protection from apoptosis. Our study supports a direct role for C3 in activating the mTOR-ribosomal biogenesis axis in glia which subsequently mediate early neuro-axonal stress and later synapse loss.

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Myeloid C3 causes neuronal injury prior to synapse loss

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Myeloid C3 causes neuronal injury prior to synapse loss [scRNA-seq]

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Myeloid C3 causes neuronal injury prior to synapse loss

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Project description:Complement component C3 mediates pathology in several CNS neurodegenerative diseases, but the cellular and molecular mechanisms leading to neuronal injury remain unclear. We examined how C3 deletion affects glial profiles and anterior visual pathway pathology in an animal model of neuroinflammation, EAE. scRNA-seq from mouse brain and optic nerve revealed that C3 expression defined disease-associated glial subtypes characterized by increased expression of genes associated with mTOR activation, cell metabolism, and translation. This was confirmed with proteomic analysis of the optic nerves of C3KO and WT EAE mice. Deletion of C3 restored glia towards homeostatic profiles. Myeloid-derived C3 mediated injury in optic nerve axons and retinal ganglion cells (RGCs) at disease peak. Our study supports a direct role for C3 in activating the mTOR-ribosomal biogenesis axis in glia which subsequently mediate early neuro-axonal stress and synapse loss.

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