PMID- 29315742
OWN - NLM
STAT- MEDLINE
DCOM- 20180524
LR  - 20180524
IS  - 1365-2230 (Electronic)
IS  - 0307-6938 (Linking)
VI  - 43
IP  - 3
DP  - 2018 Apr
TI  - Depression- and anxiety-like behaviour is related to BDNF/TrkB signalling in a 
      mouse model of psoriasis.
PG  - 254-261
LID - 10.1111/ced.13378 [doi]
AB  - BACKGROUND: The prevalence of anxiety and depression is significantly higher in 
      individuals with psoriasis than in the general population. Clinical data also 
      show that anti-anxiety and antidepression drugs can reduce skin lesions in 
      patients with psoriasis, but the actual mechanism is still poorly understood. 
      AIM: To investigate whether brain-derived neurotrophic factor (BDNF) and 
      tropomyosin receptor kinase B (TrKB) signalling plays a role in the mechanism 
      underlying psoriasis with depression and anxiety behaviours. METHODS: Expression 
      of BDNF and tropomyosin receptor kinase B (TrKB) in the K5.Stat3C mouse, an 
      animal model of psoriasis, were investigated by reverse transcription PCR and 
      Western blotting. Anxiety-like behaviours in the elevated-plus maze test and 
      changes in BDNF/TrkB that have been implicated in depression and anxiety 
      behaviours were measured. Skin lesions induced by 12-O-tetradecanoyl 
      phorbol-13-acetate (TPA) were also measured when the mice were administered 
      fluoxetine and K252a, an antagonist of TrkB. RESULTS: The antidepression and 
      anti-anxiety drug fluoxetine reduced TPA-induced skin lesions and increased 
      expression of BDNF and TrkB in K5.Stat3C mice. More importantly, the effects of 
      fluoxetine were reversed by the TrkB antagonist K252a. CONCLUSIONS: BDNF/TrkB 
      signalling participates in the pathological mechanism of depression and anxiety 
      behaviours in psoriasis. Our findings provide a new therapeutic strategy for the 
      treatment of skin lesions in psoriasis.
CI  - (c) 2018 British Association of Dermatologists.
FAU - JiaWen, W
AU  - JiaWen W
AD  - Department ofDermatology, Medical School of Xi'an Jiaotong University, Xi'an, 
      710004, Shaanxi Province, China.
FAU - Hong, S
AU  - Hong S
AD  - Department ofNeurology, Second Affiliated Hospital, Medical School of Xi'an 
      Jiaotong University, Xi'an, 710004, Shaanxi Province, China.
FAU - ShengXiang, X
AU  - ShengXiang X
AD  - Department ofDermatology, Medical School of Xi'an Jiaotong University, Xi'an, 
      710004, Shaanxi Province, China.
FAU - Jing, L
AU  - Jing L
AD  - Department ofDermatology, Medical School of Xi'an Jiaotong University, Xi'an, 
      710004, Shaanxi Province, China.
LA  - eng
PT  - Journal Article
DEP - 20180108
PL  - England
TA  - Clin Exp Dermatol
JT  - Clinical and experimental dermatology
JID - 7606847
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (Stat3 protein, mouse)
RN  - 01K63SUP8D (Fluoxetine)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Anxiety/*complications
MH  - Behavior, Animal
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Depression/*complications
MH  - Disease Models, Animal
MH  - Fluoxetine/pharmacology
MH  - Humans
MH  - Mice
MH  - Mice, Transgenic
MH  - Psoriasis/*metabolism/*psychology
MH  - Random Allocation
MH  - Receptor, trkB/*metabolism
MH  - STAT3 Transcription Factor
MH  - Signal Transduction/drug effects
EDAT- 2018/01/10 06:00
MHDA- 2018/05/25 06:00
CRDT- 2018/01/10 06:00
PHST- 2017/01/23 00:00 [accepted]
PHST- 2018/01/10 06:00 [pubmed]
PHST- 2018/05/25 06:00 [medline]
PHST- 2018/01/10 06:00 [entrez]
AID - 10.1111/ced.13378 [doi]
PST - ppublish
SO  - Clin Exp Dermatol. 2018 Apr;43(3):254-261. doi: 10.1111/ced.13378. Epub 2018 Jan 
      8.