13 August 2018 : Animal Research
Micro-RNA-137 Inhibits Tau Hyperphosphorylation in Alzheimer’s Disease and Targets the CACNA1C Gene in Transgenic Mice and Human Neuroblastoma SH-SY5Y CellsYang Jiang12ABCE, Bing Xu2BDE, Jing Chen3BCDF, Yi Sui12ABCDF, Li Ren2BF, Jing Li1BD, Huiyu Zhang1CD, Liqing Guo1DF, Xiaohong Sun1AG*
Med Sci Monit 2018; 24: ANS5635-5644
BACKGROUND: Alzheimer’s disease (AD) results in cognitive impairment. The calcium voltage-gated channel subunit alpha-1 C CACNA1C gene encodes an alpha-1 C subunit of L-type calcium channel (LTCC). The aim of this study was to investigate the role of micro-RNA-137 (miR-137) and the CACNA1C gene in APPswe/PS1ΔE9 (APP/PS1) double-transgenic AD mice and in human neuroblastoma SH-SY5Y cells.
MATERIAL AND METHODS: Six-month-old APP/PS1 double-transgenic AD mice (N=6) and age-matched normal C57BL/6 mice (N=6) underwent a Morris water maze (MWM) test, expression levels of amyloid-β (Aβ), LTCC, the CACNA1C gene, and miR-137 were measured in the rat hippocampus and cerebral cortex in both groups of mice. A luciferase assay was used to evaluate the effect of miR-137 on the expression of CACNA1C in SH-SY5Y human neuroblastoma SH-SY5Y cells. Western blotting was used to detect the CACNA1C, phosphorylated-tau (p-tau), and Aβ proteins.
RESULTS: In APP/PS1 transgenic AD mice, spatial learning and memory was significantly reduced, levels of Aβ1–40 and Aβ1–42 were increased in the serum, hippocampus, and cerebral cortex, expression levels of miR-137 were reduced, expression of CACNA1C protein was increased in the hippocampus and cerebral cortex, compared with normal control mice. miR-137 regulated the expression of the CACNA1C gene. Increased expression levels of p-tau (Ser202, Ser396, and Ser404) induced by Aβ1–42 were inhibited by miR-137 mimics in SH-SY5Y human neuroblastoma cells in vitro.
CONCLUSIONS: In a transgenic mouse model of AD, miR-137 and expression of the CACNA1C gene inhibited the hyperphosphorylation of tau protein.
Keywords: 14-3-3 Proteins, Alzheimer Disease, Amyloid beta-Peptides
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