MicroRNA-137-5p improves the condition of Alzheimer's disease by targeting USP30
Objective To explore the protective mechanism of miR-137-5p in Alzheimer's disease(AD).Methods The expressions of miR-137 and ubiquitin specific protease 30(USP30)in serum samples of AD patients and healthy controls were measured by quantitative reverse transcriptase PCR(qRT-PCR).The AD mouse model was established with D-galactose and aluminum chloride,which was verified by the water maze test to assess mouse behaviors.An in vitro AD model was created in amyloid beta 1-42(Aβ1-42)oligomer-induced SH-SY5Y cells,and the expressions of miR-137-5p and USP30 in the AD model were detected by qRT-PCR.Dual-luciferase reporter assay was performed to verify the target binding relationship between miR-137-5p and USP30.Results MiR-137-5p was downregulated in AD patients compared with that of healthy controls(P＜0.05),while USP30 was significantly upregulated(P＜0.05).MiR-137-5p improved apoptosis in the in vitro AD model,and overexpression of USP30 partially reversed the regulatory effect of miR-137-5p on Aβ1-42-induced SH-SY5Y cells.MiR-137-5p improved cognitive performance and Aβ deposition in AD mice through targeting USP30.Conclusion MiR-137-5p can improve AD symptoms by down-regulating USP30,suggesting that miR-137-5p can be a therapeutic target for the treatment of AD.
Alzheimer's diseasemiR-137-5pubiquitin specific protease 30(USP30)amyloid beta 1-42(Aβ1-42)
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维普
