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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Aβ Induces Neuroinflammation and Microglial M1 Polarization via cGAS-STING-IFITM3 Signaling Pathway in BV-2 Cells
Zheng Wu1, Wei Tang2, Fatima Elzahra E M Ibrahim1
1Department of Neurology, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Shahekou District, Dalian City, 116023, Liaoning Province, China.
Abstract:
Microglia, innate immune cells of the brain, constantly monitor the dynamic changes of the brain microenvironment under physiological conditions and respond in time. Growing evidence suggests that microglia-mediated neuroinflammation plays an important role in the pathogenesis of Alzheimer's disease. In this study, we investigated that the expression of IFITM3 was significantly upregulated in microglia under the Aβ treatment, and knockdown of IFITM3 in vitro suppressed the M1-like polarization of microglia. Moreover, IFITM3 was regulated by cGAS-STING signaling in activated microglia, and inhibition of cGAS-STING signaling reduces IFITM3 expression. Taken together, our findings suggested that the cGAS-STING-IFITM3 axis may be involved in Aβ-induced neuroinflammation in microglia.
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