Androgenetic alopecia (AGA), a hereditary disorder that involves the progressive 
thinning of hair in a defined pattern, is driven by androgens. The hair follicle 
dermal papilla (DP) expresses androgen receptors (AR) and plays an important 
role in the control of normal hair growth. In AGA, it has been proposed that the 
inhibitory actions of androgens are mediated via the DP although the molecular 
nature of these interactions is poorly understood. To investigate mechanisms of 
AGA, we cultured DP cells (DPC) from balding and non-balding scalp and confirmed 
previous reports that balding DPC grow slower in vitro than non-balding DPC. 
Loss of proliferative capacity of balding DPC was associated with changes in 
cell morphology, expression of senescence-associated beta-galactosidase, as well 
as decreased expression of proliferating cell nuclear antigen and Bmi-1; 
upregulation of p16(INK4a)/pRb and nuclear expression of markers of oxidative 
stress and DNA damage including heat shock protein-27, super oxide dismutase 
catalase, ataxia-telangiectasia-mutated kinase (ATM), and ATM- and Rad3-related 
protein. Premature senescence of balding DPC in vitro in association with 
expression of p16(INK4a)/pRB suggests that balding DPC are sensitive to 
environmental stress and identifies alternative pathways that could lead to 
novel therapeutic strategies for treatment of AGA.