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.

Základní údaje

Originální název

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

Autoři

VEREŠČÁKOVÁ, Hana (203 Česká republika), Gabriela AMBROŽOVÁ (203 Česká republika), Lukáš KUBALA (203 Česká republika), Tomáš PEREČKO (703 Slovensko), Adolf KOUDELKA (203 Česká republika, domácí), Ondřej VAŠÍČEK (203 Česká republika), T.K. RUDOLPH (276 Německo), A. KLINKE (276 Německo), S.R. WOODCOCK (840 Spojené státy), B.A. FREEMAN (840 Spojené státy) a Michaela PEKAROVÁ (703 Slovensko, garant)

Vydání

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

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10601 Cell biology

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Impakt faktor

Impact factor: 6.020

Kód RIV

RIV/00216224:14310/17:00096042

Organizační jednotka

Přírodovědecká fakulta

UT WoS

000395968300002

Klíčová slova česky

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

Klíčová slova anglicky

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

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 9. 4. 2018 16:41, Ing. Nicole Zrilić

Anotace

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.