Literature DB >> 22133888

VAP-1/SSAO plasma activity and brain expression in human hemorrhagic stroke.

Mar Hernandez-Guillamon1, Montse Solé, Pilar Delgado, Lidia García-Bonilla, Dolors Giralt, Cristina Boada, Anna Penalba, Sandra García, Alan Flores, Marc Ribó, José Alvarez-Sabin, Arantxa Ortega-Aznar, Mercedes Unzeta, Joan Montaner.   

Abstract

BACKGROUND: Vascular adhesion protein-1 (VAP-1) is a cell surface and circulating enzyme that belongs to the semicarbazide-sensitive amine oxidase (SSAO) family, which oxidatively deaminates primary amines and is implicated in leukocyte extravasation. Our aim was to investigate the alteration of soluble VAP-1/SSAO activity in plasma samples after acute intracerebral hemorrhage (ICH) and its presence in human ICH brain tissue.
METHODS: VAP-1/SSAO activity was determined in plasma of 66 ICH patients and 58 healthy controls. In addition, we assessed the expression of VAP-1/SSAO in postmortem brain tissue from hemorrhagic stroke patients by Western blot and immunohistochemistry.
RESULTS: We observed significantly higher levels of plasma VAP-1/SSAO activity in patients with ICH compared to matched elderly controls (p = 0.001). Plasma VAP-1/SSAO activity <2.7 pmol/min·mg and baseline ICH volume <17 ml were independent predictors of neurological improvement after 48 h (OR 6.8, 95% CI 1.14-41.67, p = 0.035, and OR 10.64, 95% CI 1.1-100, p = 0.041, respectively), after adjustment for baseline stroke severity. We also found that membrane-bound VAP-1/SSAO levels were lower in the perihematoma region than in the corresponding contralateral brain areas of patients deceased due to ICH (p = 0.024).
CONCLUSIONS: Our data demonstrate that plasma VAP-1/SSAO activity is increased in ICH and predicts neurological outcome, suggesting a possible contribution of the soluble protein in secondary brain damage. Furthermore, anti-VAP-1/SSAO strategies might be a promising approach to prevent neurological worsening following ICH.
Copyright © 2011 S. Karger AG, Basel.

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Year:  2011        PMID: 22133888     DOI: 10.1159/000333370

Source DB:  PubMed          Journal:  Cerebrovasc Dis        ISSN: 1015-9770            Impact factor:   2.762


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