Overexpression of Bcl-2 Protects from Ultraviolet B-Induced Apoptosis but Promotes Hair Follicle Regression and Chemotherapy-Induced Alopecia
April 2000
in “The American journal of pathology”
TLDR Bcl-2 overexpression protects against UVB damage but worsens hair loss from chemotherapy.
The study investigated the role of Bcl-2 in hair growth and keratinocyte apoptosis using transgenic mice overexpressing human Bcl-2. These K14/Bcl-2 mice exhibited significantly fewer UVB-induced apoptotic keratinocytes compared to wild-type mice, indicating protection from UVB-induced apoptosis. However, the overexpression of Bcl-2 did not affect neonatal hair follicle morphogenesis or the onset of the first wave of hair follicle regression (catagen). Instead, it accelerated spontaneous catagen progression and promoted follicular dystrophy during chemotherapy-induced alopecia. Thus, while Bcl-2 overexpression protected against UVB-induced apoptosis, it unexpectedly enhanced catagen- and chemotherapy-associated keratinocyte apoptosis.
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Cited in this study
research Principles of Hair Cycle Control
Manipulating the catagen and telogen phases of hair growth could lead to treatments for hair disorders.
research Chemotherapy-induced alopecia in mice. Induction by cyclophosphamide, inhibition by cyclosporine A, and modulation by dexamethasone.
Cyclosporine A slows down hair loss from chemotherapy in mice, while dexamethasone increases hair loss but speeds up regrowth.