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Androgen Receptor Accelerates Premature Senescence
of Human Dermal Papilla Cells in Association with DNA
Damage
Abstract
The dermal papilla, located in the hair follicle, expresses androgen receptor and plays an important role in hair growth.
Androgen/Androgen receptor actions have been implicated in the pathogenesis of androgenetic alopecia, but the exact
mechanism is not well known. Recent studies suggest that balding dermal papilla cells exhibit premature senescence,
upregulation of p16INK4a, and nuclear expression of DNA damage markers. To investigate whether androgen/AR signaling
influences the premature senescence of dermal papilla cells, we first compared frontal scalp dermal papilla cells of
androgenetic alopecia patients with matched normal controls and observed that premature senescence is more prominent
in the dermal papilla cells of androgenetic alopecia patients. Exposure of androgen induced premature senescence in
dermal papilla cells from non-balding frontal and transitional zone of balding scalp follicles but not in beard follicles.
Overexpression of the AR promoted androgen-induced premature senescence in association with p16INK4a upregulation,
whereas knockdown of the androgen receptor diminished the effects of androgen. An analysis of c-H2AX expression in
response to androgen/androgen receptor signaling suggested that DNA damage contributes to androgen/androgen
receptor-accelerated premature senescence. These results define androgen/androgen receptor signaling as an accelerator
of premature senescence in dermal papilla cells and suggest that the androgen/androgen receptor-mediated DNA damagep16
INK4a axis is a potential therapeutic target in the treatment of androgenetic alopecia.
http://www.plosone.org/article/fetc....1371/journal.pone.0079434&representation=PDF
of Human Dermal Papilla Cells in Association with DNA
Damage
Abstract
The dermal papilla, located in the hair follicle, expresses androgen receptor and plays an important role in hair growth.
Androgen/Androgen receptor actions have been implicated in the pathogenesis of androgenetic alopecia, but the exact
mechanism is not well known. Recent studies suggest that balding dermal papilla cells exhibit premature senescence,
upregulation of p16INK4a, and nuclear expression of DNA damage markers. To investigate whether androgen/AR signaling
influences the premature senescence of dermal papilla cells, we first compared frontal scalp dermal papilla cells of
androgenetic alopecia patients with matched normal controls and observed that premature senescence is more prominent
in the dermal papilla cells of androgenetic alopecia patients. Exposure of androgen induced premature senescence in
dermal papilla cells from non-balding frontal and transitional zone of balding scalp follicles but not in beard follicles.
Overexpression of the AR promoted androgen-induced premature senescence in association with p16INK4a upregulation,
whereas knockdown of the androgen receptor diminished the effects of androgen. An analysis of c-H2AX expression in
response to androgen/androgen receptor signaling suggested that DNA damage contributes to androgen/androgen
receptor-accelerated premature senescence. These results define androgen/androgen receptor signaling as an accelerator
of premature senescence in dermal papilla cells and suggest that the androgen/androgen receptor-mediated DNA damagep16
INK4a axis is a potential therapeutic target in the treatment of androgenetic alopecia.
http://www.plosone.org/article/fetc....1371/journal.pone.0079434&representation=PDF