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(American Journal of Pathology. 2001;158:1913-1919.)
© 2001 American Society for Investigative Pathology

Short Communication

p53 Involvement in the Control of Murine Hair Follicle Regression

Vladimir A. Botchkarev*, Elena A. Komarova{dagger}, Frank Siebenhaar*{ddagger}, Natalia V. Botchkareva*, Andrei A. Sharov*, Pavel G. Komarov{dagger}§, Marcus Maurer{ddagger}, Andrei V. Gudkov{dagger} and Barbara A. Gilchrest*

From the Department of Dermatology,*
Boston University School of Medicine, Boston, Massachusetts; the Department of Molecular Genetics,{dagger}
University of Illinois at Chicago, Chicago, Illinois; the Department of Dermatology,{ddagger}
Johannes Gutenberg-University, Mainz, Germany; and Quark Biotech, Inc.,§
Pleasanton, California

p53 is a transcription factor mediating a variety of biological responses including apoptotic cell death. p53 was recently shown to control apoptosis in the hair follicle induced by ionizing radiation and chemotherapy, but its role in the apoptosis-driven physiological hair follicle regression (catagen) remains to be elucidated. Here, we show that p53 protein is strongly expressed and co-localized with apoptotic markers in the regressing hair follicle compartments during catagen. In contrast to wild-type mice, p53 knockout mice show significant retardation of catagen accompanied by significant decrease in the number of apoptotic cells in the hair matrix. Furthermore, p53 null hair follicles are characterized by alterations in the expression of markers that are encoded by p53 target genes and are implicated in the control of catagen (Bax, Bcl-2, insulin-like growth factor binding protein-3). These data suggest that p53 is involved in the control of apoptosis in the hair follicle during physiological regression and imply that p53 antagonists may be useful for the management of hair growth disorders characterized by premature entry into catagen, such as androgenetic alopecia, alopecia areata, and telogen effluvium.




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