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Targeting NCAM1/FGFR1 signaling to alleviate sleep disturbance-induced neuroinflammation in the hypothalamus

ABSTRACT: Sleep disturbance is a prevalent public health concern linked to cognitive deficits and emotional dysregulation, yet the underlying mechanisms by which SD leads to hypothalamic dysfunction remain poorly understood. We demonstrated that two-week SD induced significant neuroinflammation in the hypothalamus, characterized by elevated expression of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α, as well as the chemokine Ccl2, alongside progressive neuronal loss, as evidenced by reduced nissl bodies and NeuN+ cells. Single-nucleus RNA sequencing revealed that inhibitory neurons were the most responsive hypothalamic cell cluster to SD, exhibiting enriched pro-inflammatory pathways (e.g., TNF and IL-17 signaling) and neurodegenerative transcriptional programs. Furthermore, SD triggered microglial activation and a phenotypic shift toward a disease-associated state, with enhanced antigen-presenting and pro-inflammatory capacity. Notably, intercellular communication analysis identified the neural cell adhesion molecule 1 (NCAM1)/fibroblast growth factor receptor 1 (FGFR1) signaling axis as a key mediator of crosstalk between microglia and other cell types. In vitro experiments in BV2 cells revealed that NCAM1, via FGFR1, suppressed lipopolysaccharide-induced M1 polarization and the subsequent release of pro-inflammatory cytokines. Collectively, our findings elucidate a critical protective role for the NCAM1/FGFR1 axis in mitigating SD-induced hypothalamic neuroinflammation and neuronal injury, highlighting a potential therapeutic target for sleep-related neurological disorders.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE342037 | GEO | 2026/08/07

REPOSITORIES: GEO

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