A role for p75 neurotrophin receptor in the control of apoptosis‐driven hair follicle regression

ABSTRACT To examine the mechanisms that underlie the neurotrophin‐induced, apoptosis‐driven hair follicle involution (catagen), the expression and function of p75 neurotrophin receptor (p75NTR), which is implicated in apoptosis control, were studied during spontaneous catagen development in murine s...

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Published in:The FASEB journal 2000-10, Vol.14 (13), p.1931-1942
Main Authors: Botchkarev, Vladimir A., Botchkareva, Natalia V., Albers, Kathryn M., Chen, Ling-Hong, Welker, Pia, Paus, Ralf
Format: Article
Language:English
Subjects:
alopecia
Animals
Apoptosis
BDNF
Fluorescent Antibody Technique
Hair Diseases - therapy
Hair Follicle - physiology
In Situ Nick-End Labeling
Keratinocytes - cytology
kerotinocyte catagen
Membrane Glycoproteins
Mice
Mice, Inbred C57BL
Mice, Knockout
Models, Animal
Nerve Growth Factors - genetics
Nerve Growth Factors - metabolism
NGF
NT-3
Organ Culture Techniques
p75NTR
Periodicity
Protein-Tyrosine Kinases
Receptor, Nerve Growth Factor
Receptor, trkC
Receptors, Nerve Growth Factor - genetics
Receptors, Nerve Growth Factor - metabolism
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction
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Summary:ABSTRACT To examine the mechanisms that underlie the neurotrophin‐induced, apoptosis‐driven hair follicle involution (catagen), the expression and function of p75 neurotrophin receptor (p75NTR), which is implicated in apoptosis control, were studied during spontaneous catagen development in murine skin. By RT‐PCR, high steady‐state p75NTR mRNA skin levels were found during the anagen– catagen transition of the hair follicle. By immunohistochemistry, p75NTR alone was strongly expressed in TUNEL+/Bcl2— keratinocytes of the regressing outer root sheath, but both p75NTR and TrkB and/or TrkC were expressed by the nonregressing TUNEL‐/Bcl2+ secondary hair germ keratinocytes. To determine whether p75NTR is functionally involved in catagen control, spontaneous catagen development was compared in vivo between p75NTR knockout (— /—) and wild‐type mice. There was significant catagen retardation in p75NTR knockout mice as compared to wild‐type controls (P
ISSN:0892-6638
1530-6860
DOI:10.1096/fj.99-0930com