title: Tight junctions and compression therapy in chronic venous insufficiency.
abstract: Tight junctions (TJs) provide a barrier function, inhibiting solute and water flow through the paracellular space. There had been no analysis until now as to how tight junction molecules could be involved in the pathology of patients with chronic venous insufficiency. The aim of the study was to analyse the expression pattern of TJ-molecules occludin (OCLN), claudin-1 (CLDN-1), claudin-3 (CLDN-3) and claudin-5 (CLDN-5) on mRNA and protein level in patients with edema, venous leg ulcers and healthy controls. Biopsy specimens were taken in healthy individuals and in patients before, and four weeks after compression therapy. mRNA-expression was determined by using reverse-transcriptase and polymerase chain reaction (RT-PCR) and the protein-expression was determined by Western blotting from tissue specimens. Quantification performed determining the expression for TJ-molecules displayed diminished expression for CLDN-1 (p<0.01) and CLDN-5 (p<0.01) in patients with chronic venous insufficiency in comparison with healthy controls on mRNA as well as protein level. No statistical differences were detected for OCLN and CLDN-3 between the edema group and healthy controls. There was a significantly elevated expression (p<0.01) on mRNA and protein level between the leg ulcer group and healthy controls for OCLN and CLDN-3. Densitometric evaluation revealed a more significantly elevated expression (p<0.01) for CLDN-1 and CLDN-5 on mRNA and protein level after four weeks of compression therapy in comparison with prior to treatment for the edema as well as the leg ulcer group. Compression therapy tightens the paracellular barrier via elevated expression of specific TJs and prevents thereby the progression of chronic venous insufficiency due to inhibited permeability of fluid into the perivascular tissue.
authors.affiliation: Dermato-Phlebologische Praxis, D-76530 Baden-Baden, Germany. info@herouy.de
authors.forename: Yared
authors.initials: Y
authors.lastname: Herouy
authors.forename: Birgit
authors.initials: B
authors.lastname: Kahle
authors.forename: Marco
authors.initials: M
authors.lastname: Idzko
authors.forename: Ingo
authors.initials: I
authors.lastname: Eberth
authors.forename: Johannes
authors.initials: J
authors.lastname: Norgauer
authors.forename: Felizitas
authors.initials: F
authors.lastname: Pannier
authors.forename: Eberhard
authors.initials: E
authors.lastname: Rabe
authors.forename: Michael
authors.initials: M
authors.lastname: Jünger
authors.forename: Leena
authors.initials: L
authors.lastname: Bruckner-Tuderman
mesh_terms: D001458:Bandages; D015153:Blotting, Western; D002908:Chronic Disease; D062445:Claudin-1; D062465:Claudin-3; D057167:Claudins; D004487:Edema / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D008954:Models, Biological; D062793:Occludin; D020133:Reverse Transcriptase Polymerase Chain Reaction; D019108:Tight Junctions / Q000235:genetics / Q000378:metabolism*; D016896:Treatment Outcome; D014647:Varicose Ulcer / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D014689:Venous Insufficiency / Q000235:genetics / Q000378:metabolism / Q000628:therapy*
chemical_list: C568108:CLDN1 protein, human; C491875:CLDN2 protein, human; C568122:CLDN3 protein, human; D062445:Claudin-1; D062465:Claudin-3; D057167:Claudins; D008565:Membrane Proteins; C568985:OCLN protein, human; D062793:Occludin