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

被引:19
|
作者
Verescakova, Hana [1 ]
Ambrozova, Gabriela [1 ,2 ]
Kubala, Lukas [1 ,2 ]
Perecko, Tomas [1 ,2 ]
Koudelka, Adolf [1 ,2 ,3 ]
Vasicek, Ondrej [1 ,2 ]
Rudolph, Tanja K. [4 ]
Klinke, Anna [2 ,4 ]
Woodcock, Steven R. [5 ]
Freeman, Bruce A. [5 ]
Pekarova, Michaela [1 ,2 ]
机构
[1] Acad Sci Czech Republ, Inst Biophys, Kralovopolska 135, Brno 61265, Czech Republic
[2] St Annes Univ Hosp, Ctr Biomol & Cellular Engn, Int Clin Res Ctr, Brno, Czech Republic
[3] Masaryk Univ, Dept Anim Physiol & Immunol, Brno, Czech Republic
[4] Univ Hosp Cologne, Ctr Heart, Cologne, Germany
[5] Univ Pittsburgh, Dept Pharmacol & Chem Biol, Pittsburgh, PA USA
关键词
Nitro-oleic acid; Nitro-fatty acids; Differentiation; Inflammation; Macrophages; Growth factors; Signaling pathways; COLONY-STIMULATING FACTOR; NITRATED FATTY-ACIDS; HEMATOPOIETIC STEM-CELLS; GM-CSF; TRANSCRIPTION FACTORS; MONOCYTE/MACROPHAGE DIFFERENTIATION; NITROLINOLEIC ACID; GENE-EXPRESSION; FACTOR-RECEPTOR; FACTOR-I;
D O I
10.1016/j.freeradbiomed.2017.01.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:10 / 19
页数:10
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