MiR-124-3p attenuates hyperphosphorylation of Tau protein-induced apoptosis via caveolin-1-PI3K/Akt/GSK3β pathway in N2a/APP695swe cells.

摘要: // Qingmei Kang 1, 2, * , Yue Xiang Dan Li 2 Jie Liang Xiong Zhang Fanlin Zhou Mengyuan Qiao Yingling Nie Yurong He Jingyi Cheng Yubing Dai 3 Yu 1 Department of Pathology, Chongqing Medical University, Chongqing, 400016, China Center for Molecular Medicine Testing, Neurosurgery, The Affiliated Hospital Guizhou Guiyang, Guizhou, 550004, These authors contributed equally to this work Correspondence to: Li, email: liyu100@163.com Keywords: miR-124-3p, tau, caveolin-1, PI3K/Akt/GSK3β, Alzheimer's disease Received: November 02, 2016      Accepted: January 24, 2017      Published: February 07, 2017 ABSTRACT Hyperphosphorylation Tau forming neurofibrillary tangles has been considered as a crucial event in the pathogenesis (AD). MiR-124-3p belongs microRNA (miRNA) family and was markedly decreased AD, however, functions miR-124-3p AD remain unknown. We observed that expression significantly N2a/APP695swe cells; transfection mimics not only attenuated cell apoptosis abnormal hyperphosphorylation protein without any changes total protein, but also increased levels Caveolin-1, phosphoinositide 3-kinase (PI3K), phospho-Akt (Akt-Ser473)/Akt, phospho-glycogen synthase kinase-3 beta (GSK-3β-Ser9)/GSK-3β cells. further found miR-12-3p directly targeted Caveolin-1; inhibited by regulating Caveolin-1-PI3K/Akt/GSK3β pathway AD. This study reveals may play neuroprotective role which provide new ideas therapeutic targets