Document Detail

Analysis of protease-activated receptor-1 and -2 in human scar formation.
MedLine Citation:
PMID:  17597495     Owner:  NLM     Status:  MEDLINE    
Protease-activated receptor (PAR)-1 and PAR-2 are reported to contribute to the fibrotic process in a number of organs, including lung, liver, pancreas, and kidney. The aim of this study was to localize expression and biological activity of PAR-1 and PAR-2 in normal and pathological cutaneous scars. First, we investigated the immunohistochemical expression of PAR-1 and PAR-2 proteins in a series of human normal scars (NS, n = 10), hypertrophic scars (HS, n = 10), and keloids (K, n = 10). Expression of PAR-1 and PAR-2 was observed in all types of scar. Specifically, in HS and K, diffuse PAR-1 and PAR-2 positivity was found in dermal cellular areas composed of myofibroblasts, while no or minor staining was observed in the scattered fibroblasts embedded in abundant extracellular matrix in the context of the more collagenous nodules, irrespective of the type of scar. The hyperplastic epidermis overlying K was also found to be strongly PAR-1 and PAR-2 positive, whilst in most NS and HS the epidermis was faintly to moderately stained. Second, ribonuclease protection assay on paraffin-embedded specimens showed overexpression of PAR-1 and PAR-2 mRNA in K compared to NS and HS. Third, cultured human fibroblasts exposed to TGF-beta1 expressed a myofibroblast phenotype associated with overexpression of PAR-2, while PAR-1 expression was unaffected. Intracellular Ca(2+) mobilization by PAR-2 agonists in myofibroblasts was increased as compared to fibroblasts, whereas the effect of PAR-1 agonists was unchanged. Our in vivo study indicates that PAR-1 and PAR-2 are expressed in cells involved in physiological and pathological scar formation and suggests that in vitro overexpression and exaggerated functional response of PAR-2 may play a role in the function of myofibroblasts in scar evolution from a physiological repair process to a pathological tissue response.
S Materazzi; S Pellerito; C Di Serio; M Paglierani; A Naldini; C Ardinghi; F Carraro; P Geppetti; G Cirino; M Santucci; F Tarantini; D Massi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of pathology     Volume:  212     ISSN:  0022-3417     ISO Abbreviation:  J. Pathol.     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-07-12     Completed Date:  2007-09-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0204634     Medline TA:  J Pathol     Country:  England    
Other Details:
Languages:  eng     Pagination:  440-9     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Department of Critical Care Medicine and Surgery, University of Florence, Italy. Daniela.massi@UNIFI.IT
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MeSH Terms
Calcium / metabolism
Cells, Cultured
Cicatrix / metabolism*,  pathology
Cicatrix, Hypertrophic / metabolism,  pathology
Fibroblasts / drug effects,  metabolism
Gene Expression Regulation / drug effects
Keloid / metabolism,  pathology
Middle Aged
RNA, Messenger / genetics
Receptor, PAR-1 / genetics,  metabolism*
Receptor, PAR-2 / genetics,  metabolism*
Skin / metabolism
Transforming Growth Factor beta1 / pharmacology
Wound Healing / physiology
Reg. No./Substance:
0/RNA, Messenger; 0/Receptor, PAR-1; 0/Receptor, PAR-2; 0/Transforming Growth Factor beta1; 7440-70-2/Calcium

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