INVESTIGADORES
CASTRO Claudia Magdalena
congresos y reuniones científicas
Título:
Archaeosomes improve redox and inflammatory state in cultured aortic smooth muscle cells.
Autor/es:
QUESADA, ISABEL; CEJAS, JIMENA; ARLANDI, MARCOS; CASTRO CLAUDIA; ROMERO,EDER
Lugar:
Mar del Plata
Reunión:
Congreso; LXI Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2016
Resumen:
Oxidative stress is an imbalance between reactive oxygen species (ROS) production and the antioxidant defense system. NADPH-oxidase, a potent source of superoxide anions (O2?-) in the vascular wall, is directly implicated in atherogenesis. Angiotensin II stimulates ROS production through NADPH oxidase activation. ROS regulate vascular function, modulating cell growth, apoptosis, migration, inflammation, secretion, and production of extracelular matrix. Antioxidants and agents that disrupt ROS production derived from NADPH oxidase reverse vascular remodeling, improve endothelial function and reduce inflammation. However, clinical studies on antioxidant therapies have been disappointingly negative. Nanomedicine could help solve this problem. Archaeosome vesicles (ARQ) are nanoparticles composed of polar lipids unique to the Domain Archaea. We hypothesize that ARQ possibly have antiinflammatory and antioxidant properties without the need to be decorated with specific ligands to be captured by vascular smooth muscle cells (VSMC) from the aorta artery wall. All ARQ concentrations tested were non-toxic in vitro cultivated VSMC. In basal cultured condition, we found no effect in ROS production. However, when VSMC are forced to produce ROS adding angiotensin II, ARQ prevented its increased. In addition, ARQ were able to significantly downregulate Nox4 and p47phox genes in VSMC. ARQ also tended to upregulate the anti-inflammatory adipokine Adiponectin and downregulate the pro-inflammatory adipokine Resistin. These results suggest that ARQ decrease ROS production probably by downregulating Nox4 and p47phox genes and could have an anti-inflammatory action by increasing Adiponectin mRNA levels and downregulating Resistin