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

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F17%3A00476647" target="_blank" >RIV/68081707:_____/17:00476647 - isvavai.cz</a>

  • Alternative codes found

    RIV/00159816:_____/17:00066445 RIV/00216224:14310/17:00096042

  • Result on the web

    <a href="http://dx.doi.org/10.1016/j.freeradbiomed.2017.01.003" target="_blank" >http://dx.doi.org/10.1016/j.freeradbiomed.2017.01.003</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.freeradbiomed.2017.01.003" target="_blank" >10.1016/j.freeradbiomed.2017.01.003</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

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

  • Original language description

    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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10608 - Biochemistry and molecular biology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2017

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Free Radical Biology and Medicine

  • ISSN

    0891-5849

  • e-ISSN

  • Volume of the periodical

    104

  • Issue of the periodical within the volume

    MAR2017

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    10

  • Pages from-to

    10-19

  • UT code for WoS article

    000395968300002

  • EID of the result in the Scopus database