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Statements

Subject Item
n2:RIV%2F68081707%3A_____%2F14%3A00431017%21RIV15-GA0-68081707
rdf:type
n7:Vysledek skos:Concept
dcterms:description
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. 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.
dcterms:title
Protective Effects of 10-nitro-oleic Acid in a Hypoxia-Induced Murine Model of Pulmonary Hypertension Protective Effects of 10-nitro-oleic Acid in a Hypoxia-Induced Murine Model of Pulmonary Hypertension
skos:prefLabel
Protective Effects of 10-nitro-oleic Acid in a Hypoxia-Induced Murine Model of Pulmonary Hypertension Protective Effects of 10-nitro-oleic Acid in a Hypoxia-Induced Murine Model of Pulmonary Hypertension
skos:notation
RIV/68081707:_____/14:00431017!RIV15-GA0-68081707
n3:aktivita
n10:P n10:I
n3:aktivity
I, P(ED1.100/02/0123), P(GP13-40824P)
n3:cisloPeriodika
1
n3:dodaniDat
n5:2015
n3:domaciTvurceVysledku
n4:1332139 n4:7421575 n4:6422268 n4:2555263
n3:druhVysledku
n11:J
n3:duvernostUdaju
n14:S
n3:entitaPredkladatele
n16:predkladatel
n3:idSjednocenehoVysledku
40467
n3:idVysledku
RIV/68081707:_____/14:00431017
n3:jazykVysledku
n17:eng
n3:klicovaSlova
NITRO-FATTY ACIDS; MUSCLE-CELL PROLIFERATION; ARTERIAL-HYPERTENSION
n3:klicoveSlovo
n13:MUSCLE-CELL%20PROLIFERATION n13:ARTERIAL-HYPERTENSION n13:NITRO-FATTY%20ACIDS
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[38C9FAA89520]
n3:nazevZdroje
American Journal of Respiratory Cell and Molecular Biology
n3:obor
n15:BO
n3:pocetDomacichTvurcuVysledku
4
n3:pocetTvurcuVysledku
17
n3:projekt
n8:GP13-40824P n8:ED1.100%2F02%2F0123
n3:rokUplatneniVysledku
n5:2014
n3:svazekPeriodika
51
n3:tvurceVysledku
Friedrichs, K. Freeman, B. A. Rosenkranz, S. Klinke, A. Rudolph, T. K. Kubala, Lukáš Ravekes, T. Ambrožová, Gabriela Woodcock, S. R. Rudolph, V. Kolářová, Hana Baldus, S. Moeller, A. Berlin, M. Pekarová, Michaela Schermuly, R. T. Scheu, K. M.
n3:wos
000338325300016
s:issn
1044-1549
s:numberOfPages
8