University Archives

Minoxidil is a vasodilator originally developed as an oral antihypertensive that is now widely used topically to treat androgenetic alopecia by enhancing dermal papilla cell survival, and increasing follicular blood flow. Mechanistically, it opens ATP-sensitive K+ channels, upregulates growth factors like VEGF, and activates proliferative signaling such as ERK and Akt in hair follicle cells. This work tests the idea that minoxidil also engages estrogen pathways in epithelial and skin-relevant models. Estrogen-independent squamous cell lines (SCC9, A431, HeLa, HEK293T) are used as critical controls to distinguish estrogen receptor dependent from independent actions of minoxidil. Ongoing experiments apply cellular immunofluorescence to track estrogen receptor localization, asking whether minoxidil, like estrogen, drives receptor accumulation in the nucleus of epithelial cells and how this differs across skin-derived versus breast cancer lines. Together with proliferation assays, western blot analysis of estrogen receptor and downstream effectors, this work will define how minoxidil rewires hormone-responsive signaling networks in epithelial contexts that are central to hair follicle biology and skin homeostasis.