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Microglia in the rostral ventromedial medulla mediate synaptic pruning via the C1q/C3-CR3 signaling pathway – a mechanism for the chronic orofacial pain

ABSTRACT: Microglia in the rostral ventromedial medulla mediate synaptic pruning via the C1q/C3-CR3 signaling pathway – a mechanism for the chronic orofacial pain

PROVIDER: PRJNA1213975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32073150_1.fastq.gz	Fastqsanger.gz
	SRR32073150_2.fastq.gz	Fastqsanger.gz
	SRR32073151_1.fastq.gz	Fastqsanger.gz
	SRR32073151_2.fastq.gz	Fastqsanger.gz
	SRR32073152_1.fastq.gz	Fastqsanger.gz

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Microglia in the rostral ventromedial medulla mediate synaptic pruning via the C1q/C3-CR3 signaling pathway – a mechanism for the chronic orofacial pain

Project description:The mechanism of chronic orofacial pain was investigated by examining the interaction between activated microglia, C1q and neurons in RVM of rats with orofacial pain caused by temporomandibular joint injection of CFA. The results demonstrated that the pain threshold in CFA group exhibited a continuous decline, reaching its lowest point on the third day. During the modeling process, administered daily stereotactic injections of ANX-005 and minocycline into the RVM, which resulted in a notable recovery in the rats' pain threshold and a significant increase in C1q/C3 and microglia in RVM of CFA rat. The application of ANX-005 or minocycline resulted in a reduction in the expression of C1q/C3 and microglia. Notably, the expression of excitatory presynaptic membrane markers reduced and the length and density of dendritic spines decreased on neurons in RVM. Additionally, C1q was abundantly localized on excitatory presynaptic membranes and expressed in microglial lysosomes. Treatment with ANX-005 or minocycline resulted in a reduced number of immunofluorescence colocalizations and an elevated dendritic spine density. These findings indicate that initial orofacial pain induced by CFA, microglia in RVM are involved in the pruning of excitatory presynaptic membranes through the complement C1q/C3-CR3 signaling pathway. This process results in a reduction in the proportion of excitatory synapses and a disruption in the physiological balance between RVM descending facilitation and descending inhibition. This leads to the predominance of descending facilitation in pain transmission in the RVM, which in turn facilitates the chronification of orofacial pain.

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Small intestinal γδ T17 cells promote SAE through STING/C1q-induced microglial synaptic pruning

Project description:Sepsis is a severe global health issue with high mortality rates, and sepsis-associated encephalopathy (SAE) further exacerbates this risk. While recent studies have shown the migration of gut immune cells to the lungs after sepsis, their impact on the central nervous system remains unclear. Our research demonstrates that sepsis could induce the migration of IL-7Rhigh CD8low γδ T17 cells from the small intestine to the meninges, where they secrete IL-17A, impairing mitochondrial function in microglia and activating the cGAS-STING-C1q pathway. This process is accompanied by inhibited ubiquitination of STING at the K150 site, resulting in STING accumulation and increased release of C1q-tagged hippocampal synapses, which are subsequently pruned by activated microglia. Importantly, 4-Octyl itaconate mitigates the excessive synaptic pruning by inhibiting γδ T17 cell migration and promoting STING ubiquitination, thereby alleviating SAE. Our findings reveal a novel mechanism of synaptic pruning by microglia via the cGAS-STING-C1q pathway, emphasize the critical role of gut-derived γδ T17 cell migration to the meninges in SAE, and highlight the importance of STING ubiquitination in modulating C1q-mediated excessive synaptic pruning.

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