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Activated
Skin Mast Cells Are Involved in Murine Hair Follicle Regression (Catagen) |














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Marcus Maurer,
Evalies Fischer, Bori Handjiski, Esther von Stebut, Bernd Algermissen, Assad
Bavandi, and Ralf Paus |
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Department
of Dermatology (MM, EF, BH, EvS, BA, RP), Charite, Humboldt-UniversitAdat
zu Berlin, Berlin, Germany; and Department of General Dermatology (AB),
Novartis Research Institute, Vienna, Austria |
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Increasing evidence supports
a role for mast cells (MC) in the control of tissue remodeling. Using the
cyclic growth and regression activity of the murine hair follicle (HF) as
a model, we have previously demonstrated that MC are involved in regulating
the HF transformation from resting (telogen) to active hair growth (anagen).
In the present study, we investigated the potential role of skin MC in spontaneous
HF regression (catagen), a rapid and highly controlled process of organ
involution characterized by massive epithelial cell apoptosis. By histochemistry,
immunohistochemistry, and electron microscopy, we first assessed the number,
location, and granulation status of perifollicular MC during the anagen-catagen-telogen
transformation of back skin HF. Spontaneous catagen induction was associated
with a dramatic reduction of dermal MC numbers, preceded by an increase
in the percentage of degranulated MC. In vivo, the MC-secretagogues substance
P and adrenocorticotropic hormone induced premature and dystrophic catagen
development in anagen HF, whereas inhibitors of MC degranulation retarded
normal catagen development. Comparing HF cycling in MC-deficient WBB6F1-KitW/KitWv
and congenic normal (+/+) mice, catagen development was retarded in the
virtual absence of MC. These data support the notion that MC function as
hair cycle regulators and are involved in the control of HF regression.
The mouse model employed here offers an excellent tool for dissecting the
physiologic role of MC as "central switchboards of tissue remodeling"
in developmentally regulated systems, specifically in organ involution processes.
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