Document Detail

Acute venous occlusion enhances matrix metalloprotease activity: Implications on endothelial dysfunction.
MedLine Citation:
PMID:  20923679     Owner:  NLM     Status:  MEDLINE    
Venous hypertension is associated with microvascular inflammation, restructuring, and apoptosis, but the cellular and molecular mechanisms underlying these events remain uncertain. In the present study, we tested the hypothesis that elevated venous pressure and reduction of shear stress induce elevated enzymatic activity. This activity in turn may affect endothelial surface receptors and promote their dysfunction. Using a rodent model for venous hypertension using acute venular occlusion, microzymographic techniques for enzyme detection, and immunohistochemistry for receptor labeling, we found increased activity of the matrix metalloproteases (MMPs) -1, -8, and -9 and tissue inhibitors of metalloproteases (TIMPs) -1 and -2 in both high- and low-pressure regions. In this short time frame, we also observed that elevated venule pressure led to two different fates for the vascular endothelial growth factor receptor-2 (VEGFR2); in higher-pressure upstream regions, some animals exhibited higher VEGFR2 expression, while others displayed lower levels upstream compared to their downstream counterparts with lower pressure. VEGFR2 expression was, on average, more pronounced upon application of MMP inhibitor, suggesting possible cleavage of the receptor by activated enzymes in this model. We conclude that venous pressure elevation increases enzymatic activity which may contribute to inflammation and endothelial dysfunction associated with this disease by influencing critical surface receptors.
Tom Alsaigh; Elizabeth S Pocock; John J Bergan; Geert W Schmid-Schönbein
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Publication Detail:
Type:  Journal Article     Date:  2010-10-16
Journal Detail:
Title:  Microvascular research     Volume:  81     ISSN:  1095-9319     ISO Abbreviation:  Microvasc. Res.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-10     Completed Date:  2011-05-27     Revised Date:  2014-09-17    
Medline Journal Info:
Nlm Unique ID:  0165035     Medline TA:  Microvasc Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  108-16     Citation Subset:  IM    
Copyright Information:
2010 Elsevier Inc. All rights reserved.
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MeSH Terms
Biocatalysis / drug effects
Dipeptides / pharmacology
Endothelial Cells / enzymology,  metabolism
Endothelium, Vascular / enzymology*,  metabolism,  physiopathology*
Hypertension / enzymology,  metabolism,  physiopathology
Leukocytes / enzymology
Matrix Metalloproteinase 1 / metabolism
Matrix Metalloproteinase 2 / metabolism
Matrix Metalloproteinase 3 / metabolism
Matrix Metalloproteinase 8 / metabolism
Matrix Metalloproteinase 9 / metabolism
Matrix Metalloproteinase Inhibitors
Matrix Metalloproteinases / metabolism*
Mesenteric Vascular Occlusion / enzymology*,  metabolism,  physiopathology
Mesenteric Veins / enzymology*,  metabolism,  physiopathology
Rats, Wistar
Tissue Inhibitor of Metalloproteinase-1 / metabolism
Tissue Inhibitor of Metalloproteinase-2 / metabolism
Vascular Endothelial Growth Factor Receptor-2 / metabolism
Venules / enzymology,  metabolism,  physiopathology
Grant Support
R01 HL010881/HL/NHLBI NIH HHS; R01 HL010881-41/HL/NHLBI NIH HHS; R01 HL010881-42/HL/NHLBI NIH HHS; R01 HL010881-43/HL/NHLBI NIH HHS; R01 HL010881-44/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Dipeptides; 0/Matrix Metalloproteinase Inhibitors; 0/N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide; 0/Tissue Inhibitor of Metalloproteinase-1; 127497-59-0/Tissue Inhibitor of Metalloproteinase-2; EC Endothelial Growth Factor Receptor-2; EC 3.4.24.-/Matrix Metalloproteinases; EC Metalloproteinase 3; EC Metalloproteinase 2; EC Metalloproteinase 8; EC Metalloproteinase 9; EC Metalloproteinase 1

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

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