PMID- 11023977
OWN - NLM
STAT- MEDLINE
DCOM- 20001108
LR  - 20120601
IS  - 0892-6638 (Print)
IS  - 0892-6638 (Linking)
VI  - 14
IP  - 13
DP  - 2000 Oct
TI  - A role for p75 neurotrophin receptor in the control of apoptosis-driven hair 
      follicle regression.
PG  - 1931-42
AB  - 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<0.05). Instead, transgenic mice-overexpressing NGF (promoter: K14) 
      showed substantial acceleration of catagen (P<0.001). Although NGF, brain-derived 
      neurotrophic factor (BDNF), and neurotrophin 3 (NT-3) accelerated catagen in the 
      organ-cultured skin of C57BL/6 mice, these neurotrophins failed to promote 
      catagen development in the organ-cultured p75NTR null skin. These findings 
      suggest that p75NTR signaling is involved in the control of kerotinocyte 
      apoptosis during catagen and that pharmacological manipulation of p75NTR 
      signaling may prove useful for the treatment of hair disorders that display 
      premature entry into catagen.
FAU - Botchkarev, V A
AU  - Botchkarev VA
AD  - *Department of Dermatology, Charite, Humboldt University, Berlin, Germany.
FAU - Botchkareva, N V
AU  - Botchkareva NV
FAU - Albers, K M
AU  - Albers KM
FAU - Chen, L H
AU  - Chen LH
FAU - Welker, P
AU  - Welker P
FAU - Paus, R
AU  - Paus R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - FASEB J
JT  - FASEB journal : official publication of the Federation of American Societies for 
      Experimental Biology
JID - 8804484
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - EC 2.7.10.1 (Ntrk2 protein, mouse)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, trkC)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Fluorescent Antibody Technique
MH  - Hair Diseases/therapy
MH  - Hair Follicle/*physiology
MH  - In Situ Nick-End Labeling
MH  - Keratinocytes/cytology
MH  - Membrane Glycoproteins
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Models, Animal
MH  - Nerve Growth Factors/genetics/*metabolism
MH  - Organ Culture Techniques
MH  - Periodicity
MH  - *Protein-Tyrosine Kinases
MH  - Receptor, Nerve Growth Factor
MH  - Receptor, trkC
MH  - Receptors, Nerve Growth Factor/genetics/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction
EDAT- 2000/10/12 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/10/12 11:00
PHST- 2000/10/12 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/10/12 11:00 [entrez]
AID - 14/13/1931 [pii]
AID - 10.1096/fj.99-0930com [doi]
PST - ppublish
SO  - FASEB J. 2000 Oct;14(13):1931-42. doi: 10.1096/fj.99-0930com.