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MiR-191-5pnAttenuates Tau Phosphorylation, AβnGeneration, and Neuronal Cell Death by Regulating Death-AssociatednProtein Kinase 1 MiR-191-5pn通过调节死亡相关n蛋白激酶1减弱Tau磷酸化、Aβn生成和神经元细胞死亡

Figshare Pub Date : 2022-12-01 DOI: 10.1021/acschemneuro.2c00423.s001

Long Wang (95893), Xindong Shui (12517913), Mi Zhang (42795), Yingxue Mei (12517910), Yongfang Xia (12517916), Guihua Lan (12517907), Li Hu (326656), Chen-Ling Gan (11843414), Yuan Tian (225002), Ruomeng Li (6667337), Xi Gu (2632996), Tao Zhang (43681), Dongmei Chen (124974), Tae Ho Lee (3590504)

{"title":"MiR-191-5pnAttenuates Tau Phosphorylation, AβnGeneration, and Neuronal Cell Death by Regulating Death-AssociatednProtein Kinase 1","authors":"Long Wang (95893), Xindong Shui (12517913), Mi Zhang (42795), Yingxue Mei (12517910), Yongfang Xia (12517916), Guihua Lan (12517907), Li Hu (326656), Chen-Ling Gan (11843414), Yuan Tian (225002), Ruomeng Li (6667337), Xi Gu (2632996), Tao Zhang (43681), Dongmei Chen (124974), Tae Ho Lee (3590504)","doi":"10.1021/acschemneuro.2c00423.s001","DOIUrl":"https://doi.org/10.1021/acschemneuro.2c00423.s001","url":null,"abstract":"Dysregulation of microRNAs has been implicated in diversendiseases,nincluding Alzheimer’s disease (AD). MiR-191-5p in plasma/serumnhas been identified as a novel and promising noninvasive diagnosticnbiomarker for AD. However, whether miR-191-5p is involved in AD pathogenesisnis largely unknown, and its levels in human AD brains are undetermined.nHerein, we demonstrated that miR-191-5p downregulated tau phosphorylationnat multiple AD-related sites and promoted neurite outgrowth usingnimmunoblotting, immunofluorescence, and neurite outgrowth assays.nMoreover, immunoblotting and enzyme-linked immunosorbent assays indicatednthat miR-191-5p decreased amyloid precursor protein phosphorylationnlevels and beta-amyloid (Aβ) generation. Furthermore, miR-191-5pnreduced ceramide-induced neuronal cell death analyzed by trypan bluenstaining, the in situ cell death detection kit, and Annexin V-FITC/PInflow cytometry. Next, we verified that death-associated protein kinasen1 (DAPK1) was a direct target of miR-191-5p through the dual luciferasenreporter assay and confirmed that the effects of miR-191-5p were antagonizednby restoration of DAPK1 expression. Finally, the hippocampal miR-191-5pnlevel was found to be decreased in humans with AD compared with controlsnand was inversely correlated with the DAPK1 expression level. Collectively,nthese findings suggest that miR-191-5p might exert inhibitory effectsnon tau phosphorylation, Aβ secretion, and neuronal cell deathnby directly targeting DAPK1, providing an attractive therapeutic optionnfor AD.","PeriodicalId":522127,"journal":{"name":"Figshare","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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