Neurogenic inflammation in stress-induced termination of murine hair growth is promoted by nerve growth factor

Eva Milena J. Peters, Bori Handjiski, Arne Kuhlmei, Evelin Hagen, Hannes Bielas, Armin Braun, Burghard F. Klapp, Rail Paus, Petra Clara Arck

Research output: Contribution to journalArticlepeer-review

97 Scopus citations

Abstract

Recently, we have revealed the existence of a "brain-hair follicle axis" in murine skin and have identified the neuropeptide substance P (SP) as a key mediator of stress-induced hair growth inhibition in vivo. Published evidence suggests that increased numbers of SP-immunoreactive sensory fibers, as seen in the dermis of stressed mice in anagen-catagen transition, are a result of transient high levels of nerve growth factor (NGF). Thus, we now aimed at dissecting the role of NGF in stress-triggered hair growth termination in our murine model. By real time PCR and immunohistochemistry, stress-exposed mice showed an up-regulation of NGF and its low-affinity receptor p75NTR; the NGF high-affinity receptor TrkA was moderately down-regulated. On neutralization of NGF, premature onset of catagen, apoptosis, and increased number/ activation of perifollicular mast cells and antigen-presenting cells, which reflects the skin response to stress, was significantly abrogated. Stress or subcutaneous injection of recombinant NGF (to mimic stress) resulted in an increased percentage of SP+ neurons in dorsal root ganglia, as measured by retrograde tracing. Taken together, these data suggest that NGF is a central element in the perifollicular neurogenic inflammation that develops during the murine skin response to stress and antagonizing NGF may be a promising therapeutic approach to counter the negative effect of stress on hair growth.

Original languageEnglish (US)
Pages (from-to)259-271
Number of pages13
JournalAmerican Journal of Pathology
Volume165
Issue number1
DOIs
StatePublished - Jul 2004
Externally publishedYes

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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