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Background: Wnt and transforming growth factor-[beta] (TGF-[beta]) signaling pathways are known to be involved in the pathogenesis of androgenetic alopecia (AGA). However, the way that Wnt and TGF-[beta] signaling is altered in patients with AGA and whether there exists a crosstalk between them in pathogenetic process of AGA remain unclear.

Objectives: To investigate the expression of Wnt and TGF-[beta] signaling and the crosstalk between these 2 signaling pathways in AGA.

Methods: Fifteen male patients with AGA were recruited for our research. Fifteen scalp specimens of the balding were collected from frontal areas, and 9 nonbalding were collected from occipital areas. We analyzed the expression and activation of downstream Wnt and TGF-[beta] signaling molecules in both balding and nonbalding hair follicles isolated from scalp specimens. Furthermore, we evaluated the activation of Wnt and TGF-[beta] signaling after either of them was blocked with the inhibitor in balding and nonbalding dermal papilla (DP) cells.

Results: Compared with the nonbalding counterparts, the mRNA level of Wnt10a and LEF1 was decreased. But T[beta]RI and T[beta]RII, and the protein expression of TGF-[beta]1 was elevated in balding hair follicles. To investigate the crosstalk between Wnt and TGF-[beta] signaling, we used SB431542 to inhibit the TGF-[beta] signaling in balding DP cells and found that SB431542 significantly attenuated the phosphorylation of Smad2 and Akt. However, the mRNA level of Wnt10a, LEF1, and the nuclear translocation of [beta]-catenin was increased. On the other hand, we suppressed the Wnt signaling by XAV939 in nonbalding DP cells, which displayed that the level of [beta]-catenin and LEF1 was significantly inhibited; however, the level of active TGF-[beta]1 and the phosphorylation of Smad2 and Akt were up-regulated.

Conclusions: These data indicate that crosstalk between Wnt/[beta]-catenin and TGF-[beta] signaling pathways may exist as one of the important mechanisms contributing to AGA.

Copyright (C) 2016 The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.