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Article type: Research Article
Authors: Tian, Yuana; 1; * | Song, Mingruib; 1
Affiliations: [a] Department of Anesthesiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China | [b] Department of Neurology, Shanghai Changzheng Hospital, the Second Military Medical University, Shanghai, China
Correspondence: [*] Correspondence to: Yuan Tian, Department of Anesthesiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 100 Haining Road, Hongkou District, Shanghai 200080, China. Tel.: +862163240090; Fax: +862163240090; E-mail: smr66655@sina.com.
Note: [1] These authors contributed equally to this work.
Abstract: Administration of sevoflurane (SEVO) may induce learning and memory deficits, which increases the chances of developing Alzheimer’s disease. Here, we studied the effects of SEVO exposure on rats with a focus on the role of insulin-like growth factor (IGF) signaling. SEVO exposure significantly increased neuron cell apoptosis, and caused poor performance of the rats in behavior tests, by suppressing IGF-1 receptor (IGF1R). Bioinformatic analysis predicted microRNA(miR)-223-3p as an IGF1R-binding miRNA, the level of which increased in neurons after exposure to SEVO. In vitro, miR-223-3p suppressed the translation of IGF1R in neural cells. Moreover, transfection with antisense of miR-223-3p significantly attenuated SEVO exposure-induced neuron cell apoptosis. Taken together, these data suggest that SEVO-induced miR-223-3p upregulation suppresses IGF1R to impair IGF signaling, which subsequently leads to learning and memory impairments.
Keywords: Alzheimer’s disease, IGF1R, miR-223-3p, sevoflurane
DOI: 10.3233/JAD-190596
Journal: Journal of Alzheimer's Disease, vol. 71, no. 3, pp. 825-832, 2019
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