Document Detail


Modulation of permeability and adhesion molecule expression by human choroidal endothelial cells.
MedLine Citation:
PMID:  12202538     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: The therapeutic potential of TA, an anti-inflammatory glucocorticoid, for the treatment of exudative retinopathy has been examined in several independent clinical studies. The modulation of permeability and adhesion molecule expression of an epithelial cell line has been described in vitro, with the use of cytokines and triamcinolone acetonide (TA). In the current study, the influence of proinflammatory cytokines and TA on permeability and adhesion molecule expression in human choroidal endothelial cells (CECs) was investigated. METHODS: Human CEC isolates treated with IFNgamma, TNFalpha, and TA were evaluated by flow cytometry and immunocytochemistry for expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, and major histocompatibility complex (MHC)-I and -II. The effects of IFNgamma, TNFalpha, and TA on paracellular permeability of CEC monolayers were assessed in transendothelial cell resistance (TER) assays. RESULTS: Both IFNgamma and TNFalpha significantly upregulated expression of ICAM1 and MHC-I on CECs. Expression of VCAM1 was induced after stimulation with both IFNgamma and TNFalpha, whereas expression of MHC-II was induced only by stimulation with IFNgamma. Cytokine-induced expression of ICAM1, MHC-I, and MHC-II antigen by CECs was significantly downregulated by TA. IFNgamma stimulation also increased permeability of CEC monolayers, whereas subsequent TA treatment decreased permeability of CEC monolayers. CONCLUSIONS: Human CEC isolates provide a useful in vitro model to study choroidal neovascular membrane characteristics and their potential response to pro- and anti-inflammatory agents. In addition, the results indicate that TA has the capacity to reduce adhesion molecule expression and permeability of choroidal vessels in vitro, confirming its potential as a therapeutic agent for treatment of exudative macular degeneration.
Authors:
Philip L Penfold; Li Wen; Michele C Madigan; Nicholas J C King; Jan M Provis
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  43     ISSN:  0146-0404     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  2002 Sep 
Date Detail:
Created Date:  2002-08-30     Completed Date:  2002-09-12     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3125-30     Citation Subset:  IM    
Affiliation:
Save Sight Institute and Department of Clinical Ophthalmology, University of Sydney, New South Wales, Australia. ppenfold@eye.usyd.edu.au
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MeSH Terms
Descriptor/Qualifier:
Adult
Choroid / blood supply*
Cytokines / pharmacology*
Electric Conductivity
Endothelium, Vascular / cytology,  drug effects,  metabolism*
Flow Cytometry
Fluorescent Antibody Technique, Indirect
Glucocorticoids / pharmacology*
Histocompatibility Antigens Class I / metabolism
Histocompatibility Antigens Class II / metabolism
Humans
Intercellular Adhesion Molecule-1 / metabolism*
Middle Aged
Permeability / drug effects
Triamcinolone Acetonide / pharmacology*
Up-Regulation
Vascular Cell Adhesion Molecule-1 / metabolism*
Chemical
Reg. No./Substance:
0/Cytokines; 0/Glucocorticoids; 0/Histocompatibility Antigens Class I; 0/Histocompatibility Antigens Class II; 0/Vascular Cell Adhesion Molecule-1; 126547-89-5/Intercellular Adhesion Molecule-1; 76-25-5/Triamcinolone Acetonide

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


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