J 2017

Nitro-oleic acid regulates growth factor-induced differentiation of bone marrow-derived macrophages

VEREŠČÁKOVÁ, Hana, Gabriela AMBROŽOVÁ, Lukáš KUBALA, Tomáš PEREČKO, Adolf KOUDELKA et. al.

Basic information

Original name

Nitro-oleic acid regulates growth factor-induced differentiation of bone marrow-derived macrophages

Authors

VEREŠČÁKOVÁ, Hana (203 Czech Republic), Gabriela AMBROŽOVÁ (203 Czech Republic), Lukáš KUBALA (203 Czech Republic), Tomáš PEREČKO (703 Slovakia), Adolf KOUDELKA (203 Czech Republic, belonging to the institution), Ondřej VAŠÍČEK (203 Czech Republic), T.K. RUDOLPH (276 Germany), A. KLINKE (276 Germany), S.R. WOODCOCK (840 United States of America), B.A. FREEMAN (840 United States of America) and Michaela PEKAROVÁ (703 Slovakia, guarantor)

Edition

Free Radical Biology and Medicine, NEW YORK, ELSEVIER SCIENCE INC, 2017, 0891-5849

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

10601 Cell biology

Country of publisher

United States of America

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 6.020

RIV identification code

RIV/00216224:14310/17:00096042

Organization unit

Faculty of Science

UT WoS

000395968300002

Keywords (in Czech)

Nitro-oleic acid; Nitro-fatty acids; Differentiation; Inflammation; Macrophages; Growth factors; Signaling pathways

Keywords in English

Nitro-oleic acid; Nitro-fatty acids; Differentiation; Inflammation; Macrophages; Growth factors; Signaling pathways

Tags

Tags

International impact, Reviewed
Změněno: 9/4/2018 16:41, Ing. Nicole Zrilić

Abstract

V originále

Many diseases accompanied by chronic inflammation are connected with dysregulated activation of macrophage subpopulations. Recently, we reported that nitro-fatty acids (NO2-FAs), products of metabolic and inflammatory reactions of nitric oxide and nitrite, modulate macrophage and other immune cell functions. Bone marrow cell suspensions were isolated from mice and supplemented with macrophage colony-stimulating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF) in combination with NO2-OA for different times. RAW 264.7 macrophages were used for short-term (1-5 min) experiments. We discovered that NO2-OA reduces cell numbers, cell colony formation, and proliferation of macrophages differentiated with colony-stimulating factors (CSFs), all in the absence of toxicity. In a case of GM-CSF-induced bone marrow-derived macrophages (BMMs), NO2-OA acts via downregulation of signal transducer and activator of transcription 5 and extracellular signal-regulated kinase (ERK) activation. In the case of M-CSF-induced BMMs, NO2-OA decreases activation of M-CSFR and activation of related PI3K and ERR. Additionally, NO2-OA also attenuates activation of BMMs. In aggregate, we demonstrate that NO2-OA regulates the process of macrophage differentiation and that NO2-FAs represent a promising therapeutic tool in the treatment of inflammatory pathologies linked with increased accumulation of macrophages in inflamed tissues.