Linked Life Data

19787198

Source:http://linkedlifedata.com/resource/pubmed/id/19787198

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-9-29
pubmed:abstractText
Lipodermatosclerosis refers to skin induration of the lower extremities characterized by tortuous, hyperpermeable vessels preceding venous leg ulcerations. Protein ligands and receptor tyrosine kinases that specifically regulate endothelial cell function are mainly involved in physiological as well as in disease-related angiogenesis. These ligand/receptor systems include the vascular endothelial growth factor (VEGF) and the angiopoietin (Ang) families and their receptor the tyrosine kinase with immunoglobulin-like domains (Tie-2) as well as the VEGF receptor family (VEGF-R1 and VEGF-R2). In the present study, the contribution of these endothelium-specific ligand/receptor systems in tissue samples of lipodermatosclerosis was evaluated. Our results provide evidence, that the mRNA-transcripts of VEGF (p<0.01), Ang-1 (p<0.1), Ang-2 (p<0.1) and VEGF-R1 (p<0.01) were significantly upregulated in all samples of lipodermatosclerosis in comparison with healthy skin by using reverse transcriptase-polymerase chain reaction. On protein level VEGF (p<0.01), Ang-1 (p<0.1), Ang-2 (p<0.1) and VEGF-R1 (p<0.01) were significantly elevated as well. Solely for Tie-2 and for VEGF-R2 no statistical difference could be detected on mRNA and protein level in patients with lipodermatosclerosis in comparison with healthy skin. By immunohistochemistry we confirmed upregulated protein expression for VEGF, Ang-1, Ang-2 and VEGF-R1 compared with healthy skin. Our findings strongly suggest that an imbalance between these ligand/receptor systems might contribute to the pathophysiology of advanced stages of chronic venous insufficiency. Inhibition of angiogenesis could significantly impact the tissue breakdown in lipodermatosclerosis and could hereby enable the formation of venous leg ulcerations.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1791-244X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
645-51
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Inhibition of angiogenesis in lipodermatosclerosis: implication for venous ulcer formation.
pubmed:affiliation
info@herouy.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't