ANALYSIS OF APOPTOSIS DURING HAIR FOLLICLE REGRESSION (CATAGEN)

Citation
G. Lindner et al., ANALYSIS OF APOPTOSIS DURING HAIR FOLLICLE REGRESSION (CATAGEN), The American journal of pathology, 151(6), 1997, pp. 1601-1617
Citations number
81
Language
INGLESE
art.tipo
Article
ISSN journal
0002-9440
Volume
151
Issue
6
Year of publication
1997
Pages
1601 - 1617
Database
ISI
SICI code
0002-9440(1997)151:6<1601:AOADHF>2.0.ZU;2-I
Abstract
Keratinocyte apoptosis is a central element in the regulation of hair follicle regression (catagen), yet the exact location and the control of follicular keratinocyte apoptosis remain obscure. To generate an '' apoptomap'' of the hair follicle, we have studied selected apoptosis-a ssociated parameters in the C57BL/6 mouse model for hair research duri ng normal and pharmacologically manipulated, pathological catagen deve lopment, As assessed by terminal deoxynucleotide transferase dUTP fluo rescein nick end-labeling (TUNEL) stain, apoptotic cells not only appe ared in the regressing proximal follicle epithelium but, surprisingly, were also seen in the central inner root sheath, in the bulge/isthmus region, and in the secondary germ, but never in the dermal papilla. T hese apoptosis hot spots during catagen development correlated largely with a down-regulation of the Bcl-2/Bax ratio but only poorly with th e expression patterns of interleukin-1 beta converting enzyme, p55(TNF R), and Fas/Apo-1 immunoreactivity. Instead, a higher correlation was found with p75(NTR) expression. During cyclophosphamide-induced follic le dystrophy and alopecia, massive keratinocyte apoptosis occurred in the entire proximal hair bulb, except in the dermal papilla, despite a strong up-regulation of Bar and p75(NTR) immunoreactivity. Selected r eceptors of the tumor necrosis factor/nerve growth factor family and m embers of the Bcl-2 family may also play a key role in the control of follicular keratinocyte apoptosis in situ.