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p75 Neurotrophin Receptor-Mediated Signaling Promotes Human Hair Follicle Regression (Catagen).

Peters, Eva M J; Stieglitz, Marit G; Liezman, Christiane; Overall, Rupert W; Nakamura, Motonobu; Hagen, Evelyn; Klapp, Burghard F; Arck, Petra; Paus, Ralf

The American journal of pathology. 2006;168(1):221-34.

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Abstract

Nerve growth factor (NGF) and its apoptosis-promoting low-affinity receptor (p75NTR) regulate murine hair cycling. However, it is unknown whether human hair growth is also controlled through p75NTR, its high-affinity ligand pro-NGF, and/or the growth-promoting high-affinity NGF receptor tyrosine kinase A (TrkA). In microdissected human scalp anagen hair bulbs, mRNA for NGF, pro-NGF, p75NTR, and TrkA was transcribed. Immunohistomorphometry and in situ hybridization detected strong NGF and pro-NGF expression in terminally differentiating inner root sheath keratinocytes, whereas TrkA was co-expressed with p75NTR in basal and suprabasal outer root sheath keratinocytes. During spontaneous catagen development of organ-cultured human anagen hair follicles, p75NTR mRNA levels rose, and p75NTR and pro-NGF immunoreactivity increased dramatically in involuting compartments primarily devoid of TrkA expression. Here, TUNEL(+) apoptotic cells showed prominent p75NTR expression. Joint pro-NGF/NGF administration inhibited hair shaft elongation and accelerated catagen development in culture, which was antagonized by co-administration of p75NTR-blocking antibodies. In addition, mRNA and protein expression of transforming growth factor-beta2 increased early during spontaneous catagen development, and its neutralization blocked pro-NGF/NGF-dependent hair growth inhibition. Our findings suggest that pro-NGF/NGF interacts with transforming growth factor-beta2 and p75NTR to terminate anagen in human hair follicles, implying that p75NTR blockade may alleviate hair growth disorders characterized by excessive catagen development.

Bibliographic metadata

Type of resource:
Content type:
Publication type:
Published date:
Abbreviated journal title:
ISSN:
Place of publication:
United States
Volume:
168
Issue:
1
Pagination:
221-34
Digital Object Identifier:
10.2353/ajpath.2006.050163
Pubmed Identifier:
16400025
Pii Identifier:
168/1/221
Access state:
Active

Institutional metadata

University researcher(s):

Record metadata

Manchester eScholar ID:
uk-ac-man-scw:107487
Created by:
Paus, Ralf
Created:
17th January, 2011, 16:33:31
Last modified by:
Paus, Ralf
Last modified:
18th November, 2012, 01:45:32

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