J 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 (203 Česká republika), Táňa FIDLEROVÁ (203 Česká republika), Hana VEREŠČÁKOVÁ (203 Česká republika, domácí), Adolf KOUDELKA (203 Česká republika, domácí), T.K. RUDOLPH (203 Česká republika), S.R. WOODCOCK (840 Spojené státy), B.A. FREEMAN (840 Spojené státy), Lukáš KUBALA (203 Česká republika, domácí) a Michaela PEKAROVÁ (703 Slovensko, garant, domácí)

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

Kód RIV

RIV/00216224:14310/16:00095883

Organizační jednotka

Přírodovědecká fakulta

UT WoS

000383824900009

Klíčová slova anglicky

Nitro-fatty acids; Nitro-oleic acid; Endothelial cells; Macrophages; Vascular inflammation; Endothelial-mesenchymal transition

Štítky

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.