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Abstract
Background and Aims: Previously we have demonstrated that conjugated linoleic acid (CLA) is a pro-resolving lipid mediator that induces regression of atherosclerosis in vivo via modulation of monocyte/macrophage function. microRNA-155 is a key regulator of inflammation and is induced by pro-inflammatory stimuli. miR-155 has been demonstrated to mediate pro-atherogenic effects and miR-155 deficiency in murine models is associated with reduced atherosclerotic lesion burden. Aim: To investigate the effects of CLA on miR-155 and and the downstream target, SHIP-1. To investigate the role of miR-155 on the lesion microenvironment in human plaques.
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