Document Detail


Aberrant signalling and transcription factor activation as an explanation for the defective growth control and differentiation of keratinocytes in psoriasis: a hypothesis.
MedLine Citation:
PMID:  12930288     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Psoriasis is a chronic inflammatory skin disease characterized by the accumulation of red, scaly plaques on the skin. The plaques result from hyperproliferation and incomplete differentiation of keratinocytes (KC) in a process that seems to be driven, in part by skin-infiltrating leucocytes. We believe that the KC have inherent defects in intracellular signalling which could be usefully targeted to allow the development of more effective therapies. We suggest that there are defects in the regulation of the transcription factors: signal transducer and activator of transcription (STAT-1alpha), interferon regulated factor-1 (IRF-1) and NFkappaB which lead to loss of growth and differentiation control when the cells are subjected to physico-chemical and immunological stress. We also highlight recent studies that suggest that peroxisome proliferator-activated receptors, the notch receptor and defects in calcium and other ion transporting proteins may contribute to impairment in the ability of psoriatic KC to differentiate. The role of these systems in the development of the psoriatic phenotype and tests of these hypotheses are proposed.
Authors:
R C McKenzie; E Sabin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Experimental dermatology     Volume:  12     ISSN:  0906-6705     ISO Abbreviation:  Exp. Dermatol.     Publication Date:  2003 Aug 
Date Detail:
Created Date:  2003-08-21     Completed Date:  2004-05-03     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9301549     Medline TA:  Exp Dermatol     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  337-45     Citation Subset:  IM    
Affiliation:
Epidermal Inflammation and Protection Group, Department of Dermatology, University of Edinburgh, Edinburgh, Scotland, UK. Roddie.McKenzie@ed.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Differentiation
Cell Division
DNA-Binding Proteins / metabolism
Humans
Interferon Regulatory Factor-1
Interferon-Stimulated Gene Factor 3
Keratinocytes / metabolism*,  pathology*
Membrane Proteins / metabolism
Models, Biological*
NF-kappa B / metabolism
Phosphoproteins / metabolism
Psoriasis / etiology,  metabolism*,  pathology*
Receptors, Notch
Signal Transduction
Transcription Factor AP-1 / metabolism
Transcription Factors / metabolism*
Chemical
Reg. No./Substance:
0/DNA-Binding Proteins; 0/IRF1 protein, human; 0/Interferon Regulatory Factor-1; 0/Interferon-Stimulated Gene Factor 3; 0/Membrane Proteins; 0/NF-kappa B; 0/Phosphoproteins; 0/Receptors, Notch; 0/Transcription Factor AP-1; 0/Transcription Factors; 0/gamma interferon activation factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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