Detailed Information on Publication Record
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
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.