| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10737924 | Free Radical Biology and Medicine | 2012 | 13 Pages |
Abstract
⺠MPO binds to and mediates HOCl-dependent oxidation of the subendothelial matrix. ⺠HOCl-mediated matrix oxidation disrupts cell-matrix contacts, inducing de-adhesion. ⺠De-adhesion is driven by unopposed actomyosin contractile forces. ⺠De-adhesion is linked with rapid changes in adhesion-dependent signaling. ⺠MPO alters endothelial integrity and signaling by HOCl-mediated matrix oxidation.
Keywords
PBS•NO2MLC-2HOSCNPP2Y-27632HBSSHOClFAK4-aminobenzoic acid hydrazideMPOECsNO2−Endothelial dysfunctionhypothiocyanous acidhypochlorous acidBahFree radicalsnitrogen dioxide radicalBovine aortic endothelial cellsRedox signalingExtracellular matrixMethionineHank's balanced salt solutionMETmyeloperoxidaseNitriteNitric oxidefocal adhesion kinase
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Authors
Martin D. Rees, Lei Dang, Thuan Thai, Dylan M. Owen, Ernst Malle, Shane R. Thomas,