Frontiers in immunology · 2026
miR-511-3p dysregulation-mediated AKT3/USP8 signaling imbalance: a molecular bridge between neuroinflammation and PSCI.
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Zhao Wei, Song Kangping, Yang Fen, Xiao Hui, Liu Yan, Yu Yachun, Wang Te
Аннотация
BACKGROUND: This study aims to explore the regulatory effect of miR-511-3p expression imbalance on the AKT3/USP8 signaling pathway, as well as the "molecular bridge" function of this signaling imbalance between neuroinflammation and post-stroke cognitive impairment (PSCI).
METHODS: 118 stroke patients and 80 healthy individuals were enrolled. Bioinformatics and dual-luciferase assays confirmed miR-511-3p - AKT3 interaction. Oxygen-glucose deprivation/reoxygenation (OGD/R) established a stroke inflammatory cell model. Inflammatory cytokines were measured via ELISA. RT-qPCR detected miR-511-3p, AKT3, and USP8 expressions. Correlation analysis and risk factor analysis were performed using Pearson correlation and logistic regression.
RESULTS: This study found that AKT3 was a direct target of miR-511-3p. In the neural inflammation cell model, miR-511-3p could regulate the expression of AKT3/USP8; miR-511-3p/AKT3/USP8 could regulate the inflammatory response in the inflammatory cell model. In the serum of PSCI patients, the expression of miR-511-3p and USP8 were decreased, while the expressions of AKT3 was increased, and all three were associated with the inflammatory factors of the patients. Logistic regression analysis showed that low expression of miR-511-3p and USP8 were independent risk factors for PSCI.
CONCLUSION: miR-511-3p may regulate the expression of USP8 by targeting AKT3, thereby influencing the neuroinflammatory response and participating in the occurrence and development of PSCI. miR-511-3p and USP8 may potentially serve as biomarkers and therapeutic targets for PSCI.
METHODS: 118 stroke patients and 80 healthy individuals were enrolled. Bioinformatics and dual-luciferase assays confirmed miR-511-3p - AKT3 interaction. Oxygen-glucose deprivation/reoxygenation (OGD/R) established a stroke inflammatory cell model. Inflammatory cytokines were measured via ELISA. RT-qPCR detected miR-511-3p, AKT3, and USP8 expressions. Correlation analysis and risk factor analysis were performed using Pearson correlation and logistic regression.
RESULTS: This study found that AKT3 was a direct target of miR-511-3p. In the neural inflammation cell model, miR-511-3p could regulate the expression of AKT3/USP8; miR-511-3p/AKT3/USP8 could regulate the inflammatory response in the inflammatory cell model. In the serum of PSCI patients, the expression of miR-511-3p and USP8 were decreased, while the expressions of AKT3 was increased, and all three were associated with the inflammatory factors of the patients. Logistic regression analysis showed that low expression of miR-511-3p and USP8 were independent risk factors for PSCI.
CONCLUSION: miR-511-3p may regulate the expression of USP8 by targeting AKT3, thereby influencing the neuroinflammatory response and participating in the occurrence and development of PSCI. miR-511-3p and USP8 may potentially serve as biomarkers and therapeutic targets for PSCI.