%0 Journal Article
%T TGF-¦Â dependent regulation of oxygen radicals during transdifferentiation of activated hepatic stellate cells to myofibroblastoid cells
%A Verena Proell
%A Irene Carmona-Cuenca
%A Miguel M Murillo
%A Heidemarie Huber
%A Isabel Fabregat
%A Wolfgang Mikulits
%J Comparative Hepatology
%D 2007
%I BioMed Central
%R 10.1186/1476-5926-6-1
%X We found reactive oxygen species (ROS) significantly upregulated in M1-4HSCs within 72 hours of TGF-¦Â administration. In contrast, M-HTs harbored lower intracellular ROS content than M1-4HSCs, despite of elevated NADPH oxidase activity. These observations indicated an upregulation of cellular defense mechanisms in order to protect cells from harmful consequences caused by oxidative stress. In line with this hypothesis, superoxide dismutase activation provided the resistance to augmented radical production in M-HTs, and glutathione rather than catalase was responsible for intracellular hydrogen peroxide removal. Finally, the TGF-¦Â/NADPH oxidase mediated ROS production correlated with the upregulation of AP-1 as well as platelet-derived growth factor receptor subunits, which points to important contributions in establishing antioxidant defense.The data provide evidence that TGF-¦Â induces NADPH oxidase activity which causes radical production upon the transdifferentiation of activated HSCs to M-HTs. Myofibroblastoid cells are equipped with high levels of superoxide dismutase activity as well as glutathione to counterbalance NADPH oxidase dependent oxidative stress and to avoid cellular damage.Antioxidant defense mechanisms evolved as a consequence of the aerobic lifestyle caused by the photosynthetic activity of herbal organisms, which in turn depends on the capability of oxygen reduction occurring during respiration. Reactive oxygen species (ROS) are essential for a couple of processes within the cell and play a critical role in several diseases including liver damage [1]. ROS are produced (i) by the interaction of ionizing radiation with biological molecules, (ii) during cellular respiration and (iii) by myeloperoxidase and nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase of phagocytic cells such as neutrophils and macrophages. In addition, several non-phagocytotic cell types such as hepatocytes [2] and hepatic stellate cells (HSCs) [3] have also been show
%U http://www.comparative-hepatology.com/content/6/1/1