Search results for "3-Chlorotyrosine"
showing 3 items of 3 documents
Role of endothelial cell stress in the pathogenesis of chronic heart failure.
2009
Endothelial cells are key modulators of diverse physiological processes, and their impaired function is a cause of numerous cardiovascular diseases. Under physiologic condition, the reactive oxygen and nitrogen mediators in endothelia lead to the signal propagation of the initial stimulus, by forming molecules with a longer half-life like hydrogen peroxide. Hydrogen peroxide is the focus of growing attention in endothelial biology, and consequently the enzymes involved in its generation and clearance are viewed as novel mediators of great importance. In particular, among peroxidases, myeloperoxidase is recognized as a key enzyme, capable of impairing intracellular NO reservoirs as well as p…
Oxidative stress-driven expression of myeloperoxidase in endothelial cells results in accumulation of markers of oxidative and nitrosative stress in …
2009
Endothelial cells (ECs), are able to manage with higher concentrations of ROS as well as reactive nitrogen species, respect to the other cell types. The unbalance between oxidizing species and antioxidant cellular defences has been implicated in the pathogenesis of cardiovascular diseases. While the role of MPO in the oxidative burst is well established, the effects of this enzyme on endothelial biology have only recently come to light. MPO can interact with endothelial –derived NO causing its depletion and favouring its conversion to nitrogen dioxide radical, a compound responsible of protein nitration generating 3-nitrotyrosine. Moreover, MPO is the only enzyme capable to form hypoclorous…
Oxidative stress induces myeloperoxidase expression in endocardial endothelial cells from patients with chronic heart failure.
2009
Increased oxidative stress has been implicated in the pathogenesis of a number of cardiovascular diseases. Recent findings suggest that myeloperoxidase (MPO) may play a key role in the initiation and maintenance of chronic heart failure (CHF) by contributing to the depletion of the intracellular reservoir of nitric oxide (NO). NO consumption through MPO activity may lead to protein chlorination or nitration, leading to tissue damage. Primary cultures of human endocardial endothelial cells (EEC) obtained at heart transplantation of patients with CHF and human umbilical vein endothelial cells (HUVEC) were subjected to oxidative stress by incubation with hydrogen peroxide at non lethal (60 mic…