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1
* Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA;
Department of Dermatology, University Hospital Eppendorf, University of Hamburg, D-20246 Hamburg, Germany;
Department of Dermatology, Charité, Humboldt University, Berlin, Germany;
§ Centre for Cutaneous Research, Queen Mary College, University of London, London, U.K;
¶ Department of Dermatology, Johannes-Gutenberg University, Mainz, Germany;
** Department of Dermatology, Boston University, Boston, Massachusetts 02118, USA; and
Shiseido Research Center, Yokohama, Japan
1Correspondence: Department of Dermatology, UKE, University of Hamburg, Martinistr. 52, D-20246 Hamburg, Germany. E-mail: paus{at}uke.uni-hamburg.de
The regression phase of the hair cycle (catagen) is an apoptosis-driven process accompanied by terminal differentiation, proteolysis, and matrix remodeling. As an inhibitor of keratinocyte proliferation and inductor of keratinocyte apoptosis, transforming growth factor ß1 (TGF-ß1) has been proposed to play an important role in catagen regulation. This is suggested, for example, by maximal expression of TGF-ß1 and its receptors during late anagen and the onset of catagen of the hair cycle. We examined the potential involvement of TGF-ß1 in catagen control. We compared the first spontaneous entry of hair follicles into catagen between TGF-ß1 null mice and age-matched wild-type littermates, and assessed the effects of TGF-ß1 injection on murine anagen hair follicles in vivo. At day 18 p.p., hair follicles in TGF-ß1 -/- mice were still in early catagen, whereas hair follicles of +/+ littermates had already entered the subsequent resting phase (telogen). TGF-ß1-/- mice displayed more Ki-67-positive cells and fewer apoptotic cells than comparable catagen follicles from +/+ mice. In contrast, injection of TGF-ß1 into the back skin of mice induced premature catagen development. In addition, the number of proliferating follicle keratinocytes was reduced and the number of TUNEL + cells was increased in the TGF-ß1-treated mice compared to controls. Double visualization of TGF-ß type II receptor (TGFRII) and TUNEL reactivity revealed colocalization of apoptotic nuclei and TGFRII in catagen follicles. These data strongly support that TGF-ß1 ranks among the elusive endogenous regulators of catagen induction in vivo, possibly via the inhibition of keratinocyte proliferation and induction of apoptosis. Thus, TGF-ßRII agonists and antagonists may provide useful therapeutic tools for human hair growth disorders based on premature or retarded catagen development (effluvium, alopecia, hirsutism).—Foitzik, K., Lindner, G., Mueller-Roever, S., Maurer, M., Botchkareva, N., Botchkarev, V., Handjiski, B., Metz, M., Hibino, T., Soma, T., Dotto, G. P., Paus, R. Control of murine hair follicle regression (catagen) by TGF-ß1 in vivo.
Key Words: in vivo • apoptosis • TGF-ß receptor
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