miRNA microarray profiling in patients with androgenic alopecia and the effects of miR-133b on hair growth.

Abstract Objective Androgenetic alopecia (AGA), a common alopecia, is often accompanied by abnormal expression of multiple miRNAs. This study aims to investigate abnormally expressed miRNAs in patients with AGA and their specific molecular mechanism. Methods miRNA microarray profiling and qRT-PCR validation were used to screen and verify abnormally expressed miRNAs in patients with AGA. Human hair follicles (HFs) were treated with different concentrations of dihydrotestosterone (DHT, 10−5, 10−6, 10−7 and 10−8 mol/L) for 10 days. The effects of DHT on HF growth, proliferation, and miRNA expression in cultured HFs were investigated using immunofluorescence staining and qRT-PCR. Moreover, human dermal papilla cells (HDPCs) were treated/transfected with a Wnt/β-catenin pathway activator and/or miR-133b mimic, and then the CCK-8 assay was used to evaluate HDPC proliferation. qRT-PCR and Western blotting were used to measure the expression of Versican, ALP and β-catenin Results miRNA microarray profiling identified 43 miRNAs that were significantly differentially expressed in AGA patients, and qRT-PCR verified that 8 miRNAs were significantly differentially expressed. The expression of miR-133b was abnormally high in AGA patients. DHT (10−5 mol/L) inhibited human HF growth and upregulated miR-133b expression, and DHT (10−7 mol/L) induced human HF growth and downregulated miR-133b expression. HDPC proliferation was inhibited, and the expression of β-catenin was downregulated in the miR-133b mimic-transfected group compared with the control group (P   0.05), but the expression of Versican and ALP was suppressed in the cotreatment group (P  Conclusion Our data indicated that patients with androgenic alopecia have specific miRNA expression profiles and that the abnormal expression of miR-133b may inactivate the Wnt/β-catenin pathway and ultimately regulate hair growth.