Efecto de las LDL-Ox sobre la expresión de genes relacionados al proceso inflamatorio in macrophages cells

GONZALEZ MARINA CECILIA; LEDDA, ANGELO; GRASSA, MARÍA DEL MAR; MANSILLA LAURA; TOLEDO, J. D.; ESTEVE RAFOLS, MONTSERRAT

Puerto Varas

Congreso; XII PABMB Congress, 4th Latin American Protein Society meeting (Congreso Internacional); 2013

Sociedad Bioquímica y Biología Molecular de Chile, Sociedad de Biología de Chile, Latin American Protein Society Meeting

Atherosclerosis and obesity are pathologies that share an underlying inflammatory situation influencing on the progression of both diseases. Both pathologies involve a great number of pro-inflammatory cytokines along the development of diseases. Obesity is characterized by a great infiltration of circulating monocytes in white adipose tissue where they differentiate into macrophages with predominant polarization towards M1 phenotype (pro-inflammatory). The development of atherosclerotic plaque also involves the monocyte recruitment in zones with lipid deposition or physical injury, which further differentiate into macrophages with inflammatory phenotype modulated by hormonal and lipid stimuli present in cellular medium. It has been described that oxidized LDL contributes to the polarization towards M1 phenotype, involving the activation of Toll-like 4 (TLR4) receptors. Glucocorticoids are anti-inflammatory acting in the inflammation resolution among other effects by activating macrophages by alternative M2c anti-inflammatory way. Glucocorticoids are implicated in triggering and maintaining obesity, the same as what has been postulated for atherosclerosis. At peripheral tissue level, as immune system tissues, the glucocorticoid signal could be amplified or inhibited by the enzymes activities 11β-hydroxyisteroid dehydrogenase type 1 (11βHSD1) and type 2 (11βHSDH2), respectively. The objective of the present work is to study the expression of genes implicated in inflammatory processes and the metabolism of glucocorticoids in macrophages (THP-1) exposed to oxidized LDL.