Počet záznamů: 1  

Protective Effects of 10-nitro-oleic Acid in a Hypoxia-Induced Murine Model of Pulmonary Hypertension

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    0431017 - BFÚ 2015 RIV US eng J - Článek v odborném periodiku
    Klinke, A. - Moeller, A. - Pekarová, Michaela - Ravekes, T. - Friedrichs, K. - Berlin, M. - Scheu, K.M. - Kubala, Lukáš - Kolářová, Hana - Ambrožová, Gabriela - Schermuly, R.T. - Woodcock, S.R. - Freeman, B.A. - Rosenkranz, S. - Baldus, S. - Rudolph, V. - Rudolph, T.K.
    Protective Effects of 10-nitro-oleic Acid in a Hypoxia-Induced Murine Model of Pulmonary Hypertension.
    American Journal of Respiratory Cell and Molecular Biology. Roč. 51, č. 1 (2014), s. 155-162. ISSN 1044-1549. E-ISSN 1535-4989
    Grant CEP: GA MŠMT(CZ) ED1.100/02/0123; GA ČR(CZ) GP13-40824P
    Grant ostatní: GAAV(CZ) M200041208
    Institucionální podpora: RVO:68081707
    Klíčová slova: NITRO-FATTY ACIDS * MUSCLE-CELL PROLIFERATION * ARTERIAL-HYPERTENSION
    Kód oboru RIV: BO - Biofyzika
    Impakt faktor: 3.985, rok: 2014

    Pulmonary arterial hypertension (PAH) is characterized by adverse remodeling of pulmonary arteries. Although the origin of the disease and its underlying pathophysiology remain incompletely understood, inflammation has been identified as a central mediator of disease progression. Oxidative inflammatory conditions support the formation of electrophilic fatty acid nitroalkene derivatives, which exert potent anti-inflammatory effects. The current study investigated the role of 10-nitro-oleic acid (OA-NO2) in modulating the pathophysiology of PAH in mice. Mice were kept for 28 days under normoxic or hypoxic conditions, and OA-NO2 was infused subcutaneously. Right ventricular systolic pressure (RVPsys) was determined, and right ventricular and lung tissue was analyzed. The effect of OA-NO2 on cultured pulmonary artery smooth muscle cells (PASMCs) and macrophages was also investigated. Changes in RVPsys revealed increased pulmonary hypertension in mice on hypoxia, which was significantly decreased by OA-NO2 administration. Right ventricular hypertrophy and fibrosis were also attenuated by OA-NO2 treatment.
    Trvalý link: http://hdl.handle.net/11104/0235680

     
     
Počet záznamů: 1  

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