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.Základní údaje
Originální název
Nitro-oleic acid inhibits vascular endothelial inflammatory responses and the endothelial-mesenchymal transition
Autoři
AMBROŽOVÁ, Gabriela; Táňa FIDLEROVÁ; Hana VEREŠČÁKOVÁ; Adolf KOUDELKA; T.K. RUDOLPH; S.R. WOODCOCK; B.A. FREEMAN; Lukáš KUBALA a Michaela PEKAROVÁ
Vydání
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, AMSTERDAM, ELSEVIER SCIENCE BV, 2016, 0304-4165
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
10601 Cell biology
Stát vydavatele
Nizozemské království
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 4.702
Označené pro přenos do RIV
Ano
Kód RIV
RIV/00216224:14310/16:00095883
Organizační jednotka
Přírodovědecká fakulta
UT WoS
EID Scopus
Klíčová slova anglicky
Nitro-fatty acids; Nitro-oleic acid; Endothelial cells; Macrophages; Vascular inflammation; Endothelial-mesenchymal transition
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 13. 4. 2018 14:42, Ing. Nicole Zrilić
Anotace
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.