Title:MiR-22-3p Regulates Amyloid β Deposit in Mice Model of Alzheimer's Disease by Targeting Mitogen-activated Protein Kinase 14
Volume: 16
Issue: 5
Author(s): Qiling Ji*, Xuemei Wang, Jianxin Cai, Xiangnan Du, Hui Sun and Nan Zhang
Affiliation:
- Department of Neurology, Beijing Luhe Hospital Affiliated to Capital Medical University, Beijing, 101100,China
Keywords:
Alzheimer's disease, MiR-22-3p, MAPK14, BACE1, microRNA, amyloid precursor protein.
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 enzymelinked
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 overexpression. ELISA showed that Aβ40 and Aβ42 levels
were dramatically increased in AD model, which were inhibited by miR-22-3p overexpression.
Luciferase assay and immunoblotting analysis indicated that miR-22-3p targeted and regulated
MAPK14 expression.
Conclusion: MiR-22-3p overexpression reduced Aβ deposit and alleviated AD symptoms by targeting
and regulating MAPK14 expression, which ameliorated AD symptoms.
