MiR-22-3p regulates amyloid β deposit in mice model of Alzheimer's disease by targeting mitogen-activated protein kinase 14.

MiR-22-3p regulates amyloid β deposit in mice model of Alzheimer's disease by targeting mitogen-activated protein kinase 14.
Curr Neurovasc Res. 2019 Nov 11;:
Authors: Ji Q, Wang X, Cai J, Du X, Sun H, Zhang N
Abstract
Propose: To investigate whether miR-22-3p is able to regulate AD development and its molecular mechanism. Methods: Morris water maze test was performed to test the spatial memory. Quantitative polymerase chain reaction (qPCR) was used to assess the expression level of miR-22-3p. The enzyme-linked immunosorbent assay (ELISA) was used to assess the levels of Aβ40 and Aβ42. Immunoblotting analysis was performed to detect the protein expression levels of amyloid precursor protein (APP), mitogen-activated protein kinase 14 (MAPK14) and beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1). Luciferase assay was used to identify the interaction between miR-22-3p and MAPK14. The tetrazolium dye (MTT) colorimetric assay was used to test the influence of miR-22-3p overexpression on cell viability. Flow cytometry analysis was performed to evaluate the effect of miR-22-3p overexpression on cell apoptosis. Results: Morris water maze test showed that mice model of AD had impaired spatial memory, which was able to be ameliorated by miR-22-3p overexpression. Immunoblotting analysis revealed that the protein expression levels of APP, MAPK14 and BACE1 were enhanced in AD model, which could be prevented by miR-22-3p overexpres...

Source: Current Neurovascular Research - November 10, 2019 Category: Neurology Authors: Ji Q, Wang X, Cai J, Du X, Sun H, Zhang N Tags: Curr Neurovasc Res Source Type: research