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J Invest Dermatol. 2007 Nov 8; [Epub ahead of print]Click here to read
Premature Senescence of Balding Dermal Papilla Cells In Vitro Is Associated with p16(INK4a) Expression.
Bahta AW, Farjo N, Farjo B, Philpott MP.
1Centre for Cutaneous Research, Institute of Cell and Molecular Science, Barts and The London, Queen Mary's School of Medicine and Dentistry, Queen Mary College, London, UK.
Androgenetic alopecia (Androgenetic Alopecia), 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 Androgenetic Alopecia, 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 Androgenetic Alopecia, 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 Androgenetic Alopecia.Journal of Investigative Dermatology advance online publication, 8 November 2007; doi:10.1038/sj.jid.5701147.
Premature Senescence of Balding Dermal Papilla Cells In Vitro Is Associated with p16(INK4a) Expression.
Bahta AW, Farjo N, Farjo B, Philpott MP.
1Centre for Cutaneous Research, Institute of Cell and Molecular Science, Barts and The London, Queen Mary's School of Medicine and Dentistry, Queen Mary College, London, UK.
Androgenetic alopecia (Androgenetic Alopecia), 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 Androgenetic Alopecia, 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 Androgenetic Alopecia, 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 Androgenetic Alopecia.Journal of Investigative Dermatology advance online publication, 8 November 2007; doi:10.1038/sj.jid.5701147.
