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Role of adducins in endothelial barrier formation (832.9)
Author(s) -
Kugelmann Daniela,
Radeva Mariya,
Waschke Jens
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.832.9
Subject(s) - adherens junction , tight junction , microbiology and biotechnology , cell junction , barrier function , ve cadherin , endothelial stem cell , chemistry , endothelium , actin , actin cytoskeleton , cadherin , gap junction , biophysics , cytoskeleton , cell , biology , intracellular , biochemistry , in vitro , endocrinology
Adducins tightly regulate actin dynamics which is critical for endothelial barrier function. Adducins were reported to regulate epithelial junctional remodeling by controlling the assembly of actin filaments at areas of cell‐cell contacts. Here we investigated the role of adducins for endothelial barrier regulation by using microvascular human dermal and myocardial murine endothelial cells. Transendothelial electrical resistance (TER) measurements revealed that siRNA‐mediated adducin depletion impaired endothelial barrier formation. To further test whether the peripheral localization of adducins is functionally linked with the integrity of endothelial adherens junctions, junctional remodeling was induced by a Ca2+ switch‐assay. Ca2+‐depletion disturbed both linear VE‐cadherin and adducin location along cell junctions, whereas the localization of both proteins was restored as result of Ca2+‐repletion. By using TER measurements we verified that endothelial barrier properties and junction reorganization can be effectively modulated by altering Ca2+ concentration. Thus, Ca2+‐depletion drastically reduced TER whereas Ca2+‐repletion led to recovery of endothelial barrier properties reflected in increased TER. Taken together, our results indicate that adducins maybe involved in remodeling of endothelial junctions and thereby contribute to endothelial barrier regulation.