AMBROŽOVÁ, Gabriela, Hana VEREŠČÁKOVÁ, Adolf KOUDELKA, Thorben RAVEKES, Tanja K. RUDOLPH, Anna KLINKE, Volker RUDOLPH, Bruce A. FREEMAN, Steven R. WOODCOCK, Lukáš KUBALA a Michaela PEKAROVÁ. Nitro-oleic acid modulates classical and regulatory activation of macrophages and their involvement in pro-fibrotic responses. FREE RADICAL BIOLOGY AND MEDICINE. New York, NY, USA: ELSEVIER SCIENCE INC, 2016, roč. 90, January, s. 252-260. ISSN 0891-5849. Dostupné z: https://dx.doi.org/10.1016/j.freeradbiomed.2015.11.026.
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Základní údaje
Originální název Nitro-oleic acid modulates classical and regulatory activation of macrophages and their involvement in pro-fibrotic responses
Autoři AMBROŽOVÁ, Gabriela (203 Česká republika), Hana VEREŠČÁKOVÁ (203 Česká republika, domácí), Adolf KOUDELKA (203 Česká republika, domácí), Thorben RAVEKES (276 Německo), Tanja K. RUDOLPH (276 Německo), Anna KLINKE (276 Německo), Volker RUDOLPH (276 Německo), Bruce A. FREEMAN (840 Spojené státy), Steven R. WOODCOCK (840 Spojené státy), Lukáš KUBALA (203 Česká republika) a Michaela PEKAROVÁ (703 Slovensko).
Vydání FREE RADICAL BIOLOGY AND MEDICINE, New York, NY, USA, ELSEVIER SCIENCE INC, 2016, 0891-5849.
Další údaje
Originální jazyk angličtina
Typ výsledku Článek v odborném periodiku
Obor Genetika a molekulární biologie
Stát vydavatele Spojené státy
Utajení není předmětem státního či obchodního tajemství
WWW URL
Impakt faktor Impact factor: 5.606
Kód RIV RIV/00216224:14310/16:00094207
Organizační jednotka Přírodovědecká fakulta
Doi http://dx.doi.org/10.1016/j.freeradbiomed.2015.11.026
UT WoS 000367396600023
Klíčová slova anglicky Nitro-fatty acids; Nitro-oleic acid; Macrophages; Macrophage functional specialization; Fibrosis; Inflammation
Štítky AKR, rivok
Změnil Změnila: Ing. Andrea Mikešková, učo 137293. Změněno: 11. 5. 2017 18:18.
Anotace
Inflammation is an immune response triggered by microbial invasion and/or tissue injury. While acute inflammation is directed toward invading pathogens and injured cells, thus enabling tissue regeneration, chronic inflammation can lead to severe pathologies and tissue dysfunction. These processes are linked with macrophage polarization into specific inflammatory "M1-like" or regulatory "M2-like" subsets. Nitro-fatty acids (NO2-FAs), produced endogenously as byproducts of metabolism and oxidative inflammatory conditions, may be useful for treating diseases associated with dysregulated immune homeostasis. The goal of this study was to characterize the role of nitro-oleic acid (OA-NO2) in regulating the functional specialization of macrophages induced by bacterial lipopolysaccharide or interleukin-4, and to reveal specific signaling mechanisms which can account for OA-NO2-dependent modulation of inflammation and fibrotic responses. Our results show that OA-NO2 inhibits lipopolysaccharide-stimulated production of both pro-inflammatory and immunoregulatory cytokines (including transforming growth factor-beta) and inhibits nitric oxide and superoxide anion production. OA-NO2 also decreases interleukin-4-induced macrophage responses by inhibiting arginase-I expression and transforming growth factor-beta production. These effects are mediated via downregulation of signal transducers and activators of transcription, mitogen-activated protein kinase and nuclear factor-kappa B signaling responses. Finally, OA-NO2 inhibits fibrotic processes in an in vivo model of angiotensin II-induced myocardial fibrosis by attenuating expression of alpha-smooth muscle actin, systemic transforming growth factor-beta levels and infiltration of both "M1-" and "M2-like" macrophage subsets into afflicted tissue. Overall, the electrophilic fatty acid derivative OA-NO2 modulates a broad range of "M1-" and "M2-like" macrophage functions and represents a potential therapeutic approach to target diseases associated with dysregulated macrophage subsets.
VytisknoutZobrazeno: 7. 5. 2024 05:42