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Hair Cycle Control by Estrogens: Catagen Induction via Estrogen Receptor (ER)- Is Checked by ERß Signaling

Department of Dermatology (U.O., F.C., L.M., R.P.), University Hospital Hamburg-Eppendorf, University of Hamburg, 20246 Hamburg, Germany; Department of Clinical Endocrinology (M.U.), Hannover Medical School, 30623 Hannover, Germany; Center of Biomedical Research (B.H.), Department of Internal Medicine, Charité, 10117 Berlin, Germany; Department of Dermatology (M.N.), Graduate School of Medicine, 606-8507 Kyoto, Japan; and Department of Medical Nutrition (J.I., J.-A.G.), Karolinska Institute, Novum, 14157 Huddinge, Sweden

Address all correspondence to: Ralf Paus, M.D., Department of Dermatology, University Hospital Hamburg-Eppendorf, University of Hamburg, Martinistr. 52, D-20246 Hamburg, Germany. E-mail: paus{at}uke.uni-hamburg.de.

Although 17ß-estradiol (E2) is recognized as a potent hair growth modulator, our knowledge of estrogen function, signaling, and target genes in hair biology is still very limited. Between the two recognized estrogen receptors (ERs), ER and ERß, only ER had been detected in murine skin. Here we show that ER, ERß, and ERß ins are all expressed throughout the murine hair cycle, both at the protein and RNA level, but show distinct expression patterns. We confirm that topical E2 arrests murine pelage hair follicles in telogen and demonstrate that E2 is a potent inducer of premature catagen development. The ER antagonist ICI 182.780 does not induce anagen prematurely but accelerates anagen development and wave spreading in female mice. ERß knockout mice display accelerated catagen development along with an increase in the number of apoptotic hair follicle keratinocytes. This suggests that, contrary to previous concepts, ERß does indeed play a significant role in murine hair growth control: whereas the catagen-promoting properties of E2 are mediated via ER, ERß mainly may function as a silencer of ER action in hair biology. These findings illustrate the complexity of hair growth modulation by estrogens and suggest that one key to more effective hair growth manipulation with ER ligands lies in the use of selective ER or -ß antagonists/agonists. Our study also underscores that the hair cycling response to estrogens offers an ideal model for studying the controls and dynamics of wave propagation in biological systems.

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