Contribution of tyrosin phosfatase protein DUSP1 in endothelial disfunction induced by lysophosfatidilcolina and participation in the formation of atherosclerosis plaque

Abstract

Atherosclerosis plays an essential role in the development and progression of ischaemic heart disease and stroke, as well as in other cardiovascular/metabolic diseases, such as diabetes and arterial hypertension. Even though much effort has been made to understand and reduce the negative impact of cardiovascular diseases, they are still the main cause of deaths worldwide. The build-up of lipid inside of the arterial intima is a key step to lesion formation on atherosclerosis, contributing to oxidative stress and pro-inflammatory response. The oxidative stress plays an important role in this scenario, because of it leads to oxidation of many proteins, including protein tyrosine phosphatase (PTP). PTP activity is reduced by oxidation process (irreversible/reversible), and it could result in over activation of tyrosine kinase pathway. Several cellular functions that were dysregulated in atherosclerosis can be modulated by the level of tyrosine phosphorylation, like as ROS production, migration and proliferation cellular. However, the role of PTP, specifically DUSP1, in the atheroma plaque formation and vascular cell dysfunction associated to atherosclerosis are not complete understood. Therefore, we propose to evaluate whether DUSP1 contribute to endothelial dysfunction associate to atherosclerotic processes.