Detailed Information on Publication Record
2016
Nitro-oleic acid inhibits vascular endothelial inflammatory responses and the endothelial-mesenchymal transition
AMBROŽOVÁ, Gabriela, Táňa FIDLEROVÁ, Hana VEREŠČÁKOVÁ, Adolf KOUDELKA, T.K. RUDOLPH et. al.Basic information
Original name
Nitro-oleic acid inhibits vascular endothelial inflammatory responses and the endothelial-mesenchymal transition
Authors
AMBROŽOVÁ, Gabriela (203 Czech Republic), Táňa FIDLEROVÁ (203 Czech Republic), Hana VEREŠČÁKOVÁ (203 Czech Republic, belonging to the institution), Adolf KOUDELKA (203 Czech Republic, belonging to the institution), T.K. RUDOLPH (203 Czech Republic), S.R. WOODCOCK (840 United States of America), B.A. FREEMAN (840 United States of America), Lukáš KUBALA (203 Czech Republic, belonging to the institution) and Michaela PEKAROVÁ (703 Slovakia, guarantor, belonging to the institution)
Edition
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, AMSTERDAM, ELSEVIER SCIENCE BV, 2016, 0304-4165
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
10601 Cell biology
Country of publisher
Netherlands
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 4.702
RIV identification code
RIV/00216224:14310/16:00095883
Organization unit
Faculty of Science
UT WoS
000383824900009
Keywords in English
Nitro-fatty acids; Nitro-oleic acid; Endothelial cells; Macrophages; Vascular inflammation; Endothelial-mesenchymal transition
Tags
International impact, Reviewed
Změněno: 13/4/2018 14:42, Ing. Nicole Zrilić
Abstract
V originále
Background: Inflammatory-mediated pathological processes in the endothelium arise as a consequence of the dysregulation of vascular homeostasis. Of particular importance are mediators produced by stimulated monocytes/macrophages inducing activation of endothelial cells (ECs). This is manifested by excessive soluble pro-inflammatory mediator production and cell surface adhesion molecule expression. Nitro-fatty acids are endogenous products of metabolic and inflammatory reactions that display immuno-regulatory potential and may represent a novel therapeutic strategy to treat inflammatory diseases. The purpose of our study was to characterize the effects of nitro-oleic acid (OA-NO2) on inflammatory responses and the endothelial-mesenchymal transition (EndMT) in ECs that is a consequence of the altered healing phase of the immune response. Methods: The effect of OA-NO2 on inflammatory responses and EndMT was determined in murine macrophages and murine and human ECs using Western blotting, ELISA, immunostaining, and functional assays. Results: OA-NO2 limited the activation of macrophages and ECs by reducing pro-inflammatory cytokine production and adhesion molecule expression through its modulation of STAT. MAPK and NF-kappa B-regulated signaling. OA-NO2 also decreased transforming growth factor-beta-stimulated EndMT and pro-fibrotic phenotype of ECs. These effects are related to the downregulation of Smad2/3. Conclusions: The study shows the pleiotropic effect of OA-NO2 on regulating EC-macrophage interactions during the immune response and suggests a role for OA-NO2 in the regulation of vascular endothelial immune and fibrotic responses arising during chronic inflammation. General significance: These findings propose the OA-NO2 may be useful as a novel therapeutic agent for treatment of cardiovascular disorders associated with dysregulation of the endothelial immune response. (C) 2016 Elsevier B.V. All rights reserved.