Experimental and molecular pathology · 2020
miRNA microarray profiling in patients with androgenic alopecia and the effects of miR-133b on hair growth.
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Deng Wenjia, Hu Ting, Han Le, Liu Ben, Tang Xin, Chen Haiyan, Chen Xianyan, Wan Miaojian
Аннотация
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). Wnt/β-catenin pathway activator treatment significantly promoted HDPC proliferation and upregulated the expression of β-catenin (P < 0.05). In addition, the proliferation of HDPCs was not significantly different between the group cotreated with a Wnt/β-catenin pathway activator and miR-133b mimic, and the control group (P > 0.05), but the expression of Versican and ALP was suppressed in the cotreatment group (P < 0.05) 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.
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). Wnt/β-catenin pathway activator treatment significantly promoted HDPC proliferation and upregulated the expression of β-catenin (P < 0.05). In addition, the proliferation of HDPCs was not significantly different between the group cotreated with a Wnt/β-catenin pathway activator and miR-133b mimic, and the control group (P > 0.05), but the expression of Versican and ALP was suppressed in the cotreatment group (P < 0.05) 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.