CHIABRANDO GUSTAVO ALBERTO
Congresos y reuniones científicas
Título:
ROLE OF NITRO-FATTY ACIDS IN THE REGULATION OF SCAVENGER RECEPTORS AND FOAM CELL FORMATION
Autor/es:
VAZQUEZ MM; REYES AB; ACTIS DATO V; CHIABRANDO GA; BONACCI GR
Lugar:
Mar del Plata, Provincia de Buenos Aires
Reunión:
Congreso; LI Reunión Anual Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2015
Institución organizadora:
SAIB
Resumen:
LI-P03ROLE OF NITRO-FATTY ACIDS IN THE REGULATION OF SCAVENGER RECEPTORS AND FOAM CELL FORMATIONVazquezMM; Reyes AB; Actis Dato V; Chiabrando G; Bonacci GCIBICI-CONICET. Dpto Bioquímica Clínica. Fac. Ciencias Químicas. UNC.E-mail: mvazquez@fcq.unc.edu.arNitro-fatty acids (NO2-FA) are potent lipids signaling mediators formed from nitric oxide and nitrite dependent reaction. NO2-FA modulates signaling cascades via covalent posttranslational modification (PTM) to important regulatory proteins, thus affecting downstream signaling events, such as the NF-κB, PPARγ and Keap1-Nrf2 pathways. We have previously demonstrated that macrophages form nitro-conjugated linoleic acid (NO2-CLA) under inflammatory condition and they exhibit important anti-inflammatory and cytoprotective actions in vitro and in vivo. In the present work we explored the ability of NO2-FA to modulate the expression of scavenger receptors (CD36, SRA and LRP-1) on RAW264.7 and THP-1 macrophage cell line. Nitro-oleic acid (NO2-OA) induced CD36 expression and exhibited slight effect on LRP-1 and SRA expression. This up-regulation of CD36 receptor was linked to the electrophilic activation of the antioxidant transcription factor Nrf2 by NO2-FA. Thus, uptake of modified LDL particles in macrophage treated with NO2-OA result in an increase lipid accumulation by appearance of Red Oil O positive lipids droplets compared to untreated cells. Our results indicate that NO2-FA induce foam cell formation in vitro and challenged the understanding between anti-inflammatory and anti-atherogenic action of NO2-FA during plaque formation in atherosclerosis.