Decreased expression of cytokeratin 15 and tropoelastin in men with androgenetic alopecia and its relationship with increased expression of p15/p16.

INTRODUCTION: Androgenetic alopecia (AGA) or male pattern baldness is a polygenic disease with a high prevalence in the Caucasian population, with psychosocial implications. However, the molecular mechanisms involved are unknown. The aim of this study was to assess the possible changes in protein expression of cytokeratin 15 (CK15), tropoelastin (TE) and cellular senescence markers (p15/p16) in AGA patients. MATERIAL AND METHODS: An observational, analytical and prospective cohort study was performed in 57 men with AGA (42.31 ±3.01 years). Two tissue biopsies were taken: the control area (C) and the alopecia area (A). Cell viability was assessed using scalp explants from the patients, maintaining explants long term (90 days). Protein expression analysis was performed by immunohistochemistry by detecting antigen-antibody reactions (avidin-biotin complex). RESULTS: The results showed a significantly higher percentage of dead cells in area A (17.00 ±1.09% C vs. 28.50 ±1.41% A, *p < 0.05). The area affected by alopecia showed significantly lower CK15 and TE protein expression in hair follicles, sebaceous glands and epidermis (*p < 0.05). Expression of the senescence marker p15/p16 was significantly higher in hair follicles, hair bulbs and the epidermis (*p < 0.05). CONCLUSIONS: The results suggest that patients with AGA suffer tissue damage that affects different components of hair follicle stem cells as well as the extracellular matrix itself.