Botulinum Toxin Type A Alleviates Androgenetic Alopecia by Inhibiting Apoptosis of Dermal Papilla Cells via Targeting circ_0135062/miR-506-3p/Bax Axis

Abstract

Botulinum toxin type A (BTXA) has been shown to be effective in androgenetic alopecia (AGA), but its effect on dermal papillary cell (DPC) apoptosis is not yet clear. Non-coding RNA plays pivotal roles in the development of AGA. In this study, we investigated the molecular mechanism of BTXA in dihydrotestosterone(DHT)-induced apoptosis of DPCs. The expressions of circ_0135062, miR-506-3p and Bax were detected by qRT-PCR. RNA pulldown and dual luciferase assays were used to analyze binding evidence. Cell viability was validated using the cell counting kit-8 assay, and cell apoptosis was determined by ow cytometry, TUNEL assay, and Western blot. Our results revealed that BTXA inhibited apoptosis of DPCs treated with DHT and that overexpression of circ_0135062 antagonized the protection of BTXA in DHT-treated DPCs. The miR-506-3p interacted with Bax, and miR-506-3p inhibited apoptosis of DPCs against DHT-mediated damage by silencing Bax. Additionally, circ_0135062 served as a miR-506-3p sponge and inhibited miR-506-3p targeting Bax expression. In conclusion, BTXA exerted an antiapoptotic effect on DHT-induced DPC injury via the circ_0135062/miR-506-3p/Bax axis.

Intradermal Injection in Balding Region Versus Intramuscular Injection in Surrounding Muscles: A Split-Scalp, Randomized Trial on BoNT for Androgenetic Alopecia

“…By suppressing TGFβ1 secretion, BoNT effectively counters one of the principal pathophysiological processes contributing to AGA, alleviating the inhibition of follicular cell growth [ 8 ]. Furthermore, contemporary research has shed light on the role of BoNT in mitigating DHT-induced DPC dysfunction [ 22 ]. By downregulating the expression of circ_0135062, BoNT modulates miR-506-3p-targeted Bax levels, reducing apoptosis in DHT-treated DPCs [ 22 ].…”

“…Furthermore, contemporary research has shed light on the role of BoNT in mitigating DHT-induced DPC dysfunction [ 22 ]. By downregulating the expression of circ_0135062, BoNT modulates miR-506-3p-targeted Bax levels, reducing apoptosis in DHT-treated DPCs [ 22 ].…”