Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 May 4;21(2):495-504.
doi: 10.5114/aoms.2020.94914. eCollection 2025.

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

Miguel A Ortega  1   2 , María J Álvarez-Rocha  1 , Ángel Asúnsolo  2   3 , Beatriz Romero  2 , Santiago Coca  1   2 , Melchor Álvarez-Mon  1   2   4 , Julia Buján  1   2 , Natalio García-Honduvilla  1   2
Affiliations

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

Miguel A Ortega et al. Arch Med Sci. .

Abstract

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.

Keywords: androgenetic alopecia; cellular senescence; cytokeratin 15; extracellular matrix; tropoelastin.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Quantification of the percentage of dead cells in cell culture at 90 days in the control area (C) and in the area with alopecia (A). p < 0.05 (*). B, C – Representative images of cell morphology under in vitro conditions at 90 days in the control area (B) and in the area with alopecia (C)
Figure 2
Figure 2
Protein expression of cytokeratin 15 (CK15) in the hair follicle (HF), hair bulb (HB), sebaceous gland (SG) and epidermis (EP) in the control area (C) and in the area with alopecia (A). p < 0.05 (*). Protein expression images of CK15 in the HF and HB of the control area (A–C) and area with alopecia (E), as well as in the EP of area C (D) and A (F). Arrow: immunoprecipitated
Figure 3
Figure 3
Protein expression of tropoelastin (TE) in the hair follicle (HF), hair bulb (HB), sebaceous gland (SG) and epidermis (EP) in the control area (C) and in the area with alopecia (A). p < 0.05 (*) Protein expression images of TE in the HF and HB of the control area (A, B) and in the affected area (D, E), as well as in the EP of area C (C) and A (F). Arrow: immunoprecipitated
Figure 4
Figure 4
Protein expression of senescence markers (p15/p16) in the hair follicle (HF), hair bulb (HB), sebaceous gland (SG) and epidermis (EP) in the control area (C) and in the area with alopecia (A). p < 0.05 (*) Protein expression images of p15/ p16 in the HF and HB of the control area (B) and in the affected area (C–E), as well as in the EP in area C (A) and A (F). Arrow: immunoprecipitated
See this image and copyright information in PMC

Similar articles

See all similar articles

References

    1. Paus R, Olsen EA, Messenger AG. Hair growth disorders. In: Fitzpatrick’s Dermatology in General Medicine. 7th ed. Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller As, Leffell DJ (eds.). USA: The McGraw-Hill Companies Inc. 2008; 753-77.
    1. Lolli F, Pallotti F, Rossi A, et al. . Androgenetic alopecia: a review. Endocrine 2017; 57: 9-17. - PubMed
    1. Severi G, Sinclair R, Hopper JL, et al. . Androgenetic alopecia in men aged 40–69 years: prevalence and risk factors. Br J Dermatol 2003; 149: 1207-13. - PubMed
    1. Khumalo NP, Jessop S, Gumedze F, Ehrlich R. Hairdressing and the prevalence of scalp disease in African adults. Br J Dermatol 2007; 157: 981-8. - PubMed
    1. Hunt N, McHale S. The psychological impact of alopecia. BMJ 2005; 331: 951-3. - PMC - PubMed