Document Detail


Expression of adhesion molecules and cytokines on saphenous veins in chronic venous insufficiency.
MedLine Citation:
PMID:  10990550     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The objective of this study was to assess the relationship of signaling molecules to monocyte/ macrophages as a precursor to venous valve and venous wall dysfunction in patients with varicose veins. One of the hallmarks of venous dysfunction is destruction of venous valves with subsequent reflux and elevation of distal venous pressure. We recently observed that monocytes/macrophages migrate into the venous walls and valves of patients with venous insufficiency. There, they may play a role in the pathogenesis of primary venous insufficiency. If so, an important element in their performance would be the interaction between the monocytes and the endothelium as a precursor of damage to venous valves and the venous wall. To explore this interaction, immunohistochemistry was carried out to detect adhesion molecules and cytokines in surgical specimens removed during surgical therapy. Twenty-four surgical specimens consisting of proximal saphenous vein and subterminal valve were obtained using minimally traumatic technique in 6 males and 18 females who ranged in age from 31 to 79 years. Reflux was confirmed preoperatively by duplex technique, and severity was classified by the CEAP classification of the American Venous Forum. Ten patient limbs were class 2, eight were class 3, four were class 4, and two were class 6. The venous specimens were labeled using monoclonal antibody against ICAM-1, E-selectin, IL-1alpha, and TNF-alpha. CD68 was used for detection of monocytes/macrophages. Our results indicate that not only luminal venous endothelium but also endothelium in the vasa vasora of refluxing saphenous veins is activated, as indicated by the up-regulation of ICAM-1. However, IL-1alpha and TNF-alpha were increased in only selected specimens and are mainly detected in the vein wall. The factors that serve as trigger mechanisms to activate cells in the pathogenesis of primary venous dysfunction remain to be explored.
Authors:
S Takase; J J Bergan; G Schmid-Schönbein
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Annals of vascular surgery     Volume:  14     ISSN:  0890-5096     ISO Abbreviation:  Ann Vasc Surg     Publication Date:  2000 Sep 
Date Detail:
Created Date:  2001-02-02     Completed Date:  2001-02-02     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8703941     Medline TA:  Ann Vasc Surg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  427-35     Citation Subset:  IM    
Affiliation:
Department of Surgery II, Fukushima Medical University School of Medicine, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Antigens, CD / biosynthesis
Antigens, Differentiation, Myelomonocytic / biosynthesis
Cell Adhesion Molecules / biosynthesis*
Chronic Disease
Cytokines / biosynthesis*
Endothelium, Vascular / metabolism
Female
Humans
Intercellular Adhesion Molecule-1 / biosynthesis
Male
Middle Aged
Venous Insufficiency / metabolism*
Grant Support
ID/Acronym/Agency:
HL 43026/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD; 0/Antigens, Differentiation, Myelomonocytic; 0/CD68 antigen, human; 0/Cell Adhesion Molecules; 0/Cytokines; 126547-89-5/Intercellular Adhesion Molecule-1

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