Towards Defining the Pathogenesis of the Hairless Phenotype

The study investigated the pathogenesis of the hairless phenotype in HRS/J hairless mice, focusing on the mutation of the hairless (hr) gene. This mutation caused abnormalities during the first hair follicle regression (catagen), leading to complete baldness. The research revealed that in hr skin, only two epithelial cell populations in the distal outer root sheath (ORS) retained integrity, while the rest disintegrated. The surviving distal ORS formed utriculi, and remnants of the bulge retained the ability to proliferate, producing epithelial outgrowths or dermal cysts. The study suggested that the hr mutation disrupted key functional tissue units in hair follicles, possibly due to dysregulated apoptosis or impaired cell adhesion, while the distal follicle epithelium remained largely unaffected. The findings provided insights into the molecular and cellular consequences of the hr gene mutation, offering a model for understanding hair follicle integrity during catagen.