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TmEm16F may be a new therapeutic target for Alzheimer's disease

Neural Regeneration Research 2023年第3期18卷 643-651页

作者： Zhi-Qiang Cui Xiao-Ying Hu Tuo Yang Jing-Wei Guan Ying Gu Hui-Yuan Li Hui-Yu Zhang Qing-Huan Xiao Xiao-Hong Sun Department of Neurology The Fourth Affiliated Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Department of Ion Channel Pharmacology School of PharmacyChina Medical UniversityShenyangLiaoning ProvinceChina

TmEm16F is involved in many physiological processes such as blood coagulation,cell membrane fusion and bone mineralization.Activation of TmEm16F has been studied in various central nervous system diseases.High TmEm16F level has been also found to participate in microglial phagocytosis and transformation.microglia-mediated neuroinflammation is a key factor in promoting the progression of Alzheimer’s disease.However,few studies have examined the effects of TmEm16F on neuroinflammation in Alzheimer’s disease.In this study,we established TmEm16F-knockdown AD model in vitro and in vivo to investigate the underlying regulatory mechanism about TmEm16F-mediated neuroinflammation in AD.We performed a morris water maze test to evaluate the spatial memory ability of animals and detected markers for the microglia m1/m2 phenotype and NLRP3 inflammasome.Our results showed that TmEm16F was elevated in 9-month-old APP/PS1 mice.After TmEm16F knockdown in mice,spatial memory ability was improved,microglia polarization to the m2 phenotype was promoted,NLRP3 inflammasome activation was inhibited,cell apoptosis and Aβplaque deposition in brain tissue were reduced,and brain injury was alleviated.We used amyloid-beta(Aβ_(25-35))to stimulate human microglia to construct microglia models of Alzheimer’s disease.The levels of TmEm16F,inducible nitric oxide synthase(iNOS),proinflammatory cytokines and NLRP3 inflammasome-associated biomarkers were higher in Aβ_(25-35) treated group compared with that in the control group.TmEm16F knockdown enhanced the expression of the m2 phenotype biomarkers Arg1 and Socs3,reduced the release of proinflammatory factors interleukin-1,interleukin-6 and tumor necrosis factor-α,and inhibited NLRP3 inflammasome activation through reducing downstream proinflammatory factors interleukin-1βand interleukin-18.This inhibitory effect of TmEm16F knockdown on m1 microglia was partially reversed by the NLRP3 agonist Nigericin.Our findings suggest that TmEm16F participates in neuroinflammation in Alzheimer’s disease throu

关键词： Alzheimer’s disease Aβplaque inflammatory cytokines M1 phenotype m2 phenotype microglia polarization neuroinflammation NLRP3 inflammasome siRNA TmEm16F

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