Aβ Induces Neuroinflammation and Microglial M1 Polarization via cGAS-STING-IFITM3 Signaling Pathway in BV-2 Cells

Neurochemical Research - Tập 48 - Trang 2881-2894 - 2023
Zheng Wu1, Wei Tang2, Fatima Elzahra E. M. Ibrahim1, Xuejing Chen1, Hongting Yan1, Chunmei Tao1, Zhiming Wang1, Yunchu Guo1, Yu Fu1, Qi Wang3, Yusong Ge1
1Department of Neurology, the Second Hospital of Dalian Medical University, Dalian City, China
2Department of Anatomy, College of Basic Medicine, Dalian Medical University, Dalian City, China
3Department of Respiratory Medicine, The Second Hospital of Dalian Medical University, Dalian City, China

Tóm tắt

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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