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Herwig, Martina C.; Tsokos, Michael; Hermanns, M. Iris; Kirkpatrick, C. James; Müller, Annette M.

Vascular Endothelial Cadherin Expression in Lung Specimens of Patients with Sepsis-Induced Acute Respiratory Distress Syndrome and Endothelial Cell Cultures

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  • Media type: E-Article
  • Title: Vascular Endothelial Cadherin Expression in Lung Specimens of Patients with Sepsis-Induced Acute Respiratory Distress Syndrome and Endothelial Cell Cultures
  • Contributor: Herwig, Martina C.; Tsokos, Michael; Hermanns, M. Iris; Kirkpatrick, C. James; Müller, Annette M.
  • imprint: S. Karger AG, 2013
  • Published in: Pathobiology
  • Language: English
  • DOI: 10.1159/000347062
  • ISSN: 1015-2008; 1423-0291
  • Keywords: Cell Biology ; Molecular Biology ; General Medicine ; Pathology and Forensic Medicine
  • Origination:
  • Footnote:
  • Description: <jats:p>&lt;b&gt;&lt;i&gt;Aims:&lt;/i&gt;&lt;/b&gt; Vascular endothelial (VE) cadherin is a cell adhesion molecule localized at endothelial cell (EC) junctions. As a major component of endothelial adherens junctions, its main function is the maintenance and regulation of EC integrity. In the acute respiratory distress syndrome (ARDS), increased vascular permeability is a major mechanism in pulmonary edema and lung dysfunction. In this study, VE-cadherin expression was investigated in ARDS lungs and control tissue as well as in an ARDS cell culture model. &lt;b&gt;&lt;i&gt;Methods:&lt;/i&gt;&lt;/b&gt; Lung specimens of patients with ARDS due to Gram-negative sepsis (n = 20; control lung tissue: n = 41) and cell cultures of human pulmonary microvascular ECs and human umbilical vein ECs stimulated with LPS, TNF-α and IFN-&amp;#947; were stained with a VE-cadherin antibody. Staining intensity was semiquantitatively evaluated by conventional light and immunofluorescence microscopy. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; VE-cadherin expression was statistically significantly reduced in the endothelium of all vessel types in ARDS lungs compared to control tissue. Cell cultures showing disrupted cellular borders confirmed these results. &lt;b&gt;&lt;i&gt;Conclusion:&lt;/i&gt;&lt;/b&gt; Reduced expression of VE-cadherin has to be considered as a major mechanism of increased vessel permeability in ARDS. The previously described vessel-type-specific expression pattern of VE-cadherin in the human lung is not influenced by ARDS.</jats:p>